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41.5: Hormonal Control of Osmoregulatory Functions - Biology

41.5: Hormonal Control of Osmoregulatory Functions - Biology


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41.5: Hormonal Control of Osmoregulatory Functions

Hormonal Control of Osmoregulatory Functions

While the kidneys operate to maintain osmotic balance and blood pressure in the body, they also act in concert with hormones. Hormones are small molecules that act as messengers within the body. Hormones are typically secreted from one cell and travel in the bloodstream to affect a target cell in another portion of the body. Different regions of the nephron bear specialized cells that have receptors to respond to chemical messengers and hormones. [link] summarizes the hormones that control the osmoregulatory functions.

Hormones That Affect Osmoregulation
Hormone Where produced Function
Epinephrine and Norepinephrine Adrenal medulla Can decrease kidney function temporarily by vasoconstriction
Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen
Angiotensin Liver Angiotensin II affects multiple processes and increases blood pressure
Aldosterone Adrenal cortex Prevents loss of sodium and water
Anti-diuretic hormone (vasopressin) Hypothalamus (stored in the posterior pituitary) Prevents water loss
Atrial natriuretic peptide Heart atrium Decreases blood pressure by acting as a vasodilator and increasing glomerular filtration rate decreases sodium reabsorption in kidneys

Epinephrine and Norepinephrine

Epinephrine and norepinephrine are released by the adrenal medulla and nervous system respectively. They are the flight/fight hormones that are released when the body is under extreme stress. During stress, much of the body’s energy is used to combat imminent danger. Kidney function is halted temporarily by epinephrine and norepinephrine. These hormones function by acting directly on the smooth muscles of blood vessels to constrict them. Once the afferent arterioles are constricted, blood flow into the nephrons stops. These hormones go one step further and trigger the renin-angiotensin-aldosterone system.

Renin-Angiotensin-Aldosterone

The renin-angiotensin-aldosterone system, illustrated in [link] proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

Mineralocorticoids

Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. Aldosterone is a mineralocorticoid that regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. Because sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels but also the water levels in body fluids. In contrast, the aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. In contrast, absence of aldosterone means that no sodium gets reabsorbed in the renal tubules and all of it gets excreted in the urine. In addition, the daily dietary potassium load is not secreted and the retention of K + can cause a dangerous increase in plasma K + concentration. Patients who have Addison's disease have a failing adrenal cortex and cannot produce aldosterone. They lose sodium in their urine constantly, and if the supply is not replenished, the consequences can be fatal.

Antidiurectic Hormone

As previously discussed, antidiuretic hormone or ADH (also called vasopressin), as the name suggests, helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus and is stored and released from the posterior pituitary. It acts by inserting aquaporins in the collecting ducts and promotes reabsorption of water. ADH also acts as a vasoconstrictor and increases blood pressure during hemorrhaging.

Atrial Natriuretic Peptide Hormone

The atrial natriuretic peptide (ANP) lowers blood pressure by acting as a vasodilator. It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release, and because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.

Section Summary

Hormonal cues help the kidneys synchronize the osmotic needs of the body. Hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate the needs of the body as well as the communication between the different organ systems.


Epinephrine and norepinephrine

Epinephrine and norepinephrine are released by the adrenal medulla and nervous system respectively. They are the flight/fight hormones that are released when the body is under extreme stress. During stress, much of the body&rsquos energy is used to combat imminent danger. Kidney function is halted temporarily by epinephrine and norepinephrine. These hormones function by acting directly on the smooth muscles of blood vessels to constrict them. Once the afferent arterioles are constricted, blood flow into the nephrons stops. These hormones go one step further and trigger the renin-angiotensin-aldosterone system.


Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. Aldosterone is a mineralocorticoid that regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. Because sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels but also the water levels in body fluids. In contrast, the aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. In contrast, absence of aldosterone means that no sodium gets reabsorbed in the renal tubules and all of it gets excreted in the urine. In addition, the daily dietary potassium load is not secreted and the retention of K + can cause a dangerous increase in plasma K + concentration. Patients who have Addison’s disease have a failing adrenal cortex and cannot produce aldosterone. They lose sodium in their urine constantly, and if the supply is not replenished, the consequences can be fatal.

Hormonal cues help the kidneys synchronize the osmotic needs of the body. Hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate the needs of the body as well as the communication between the different organ systems.


219 Hormonal Control of Osmoregulatory Functions

By the end of this section, you will be able to do the following:

  • Explain how hormonal cues help the kidneys synchronize the osmotic needs of the body
  • Describe how hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate waste elimination, maintain correct osmolarity, and perform other osmoregulatory functions

While the kidneys operate to maintain osmotic balance and blood pressure in the body, they also act in concert with hormones. Hormones are small molecules that act as messengers within the body. Hormones are typically secreted from one cell and travel in the bloodstream to affect a target cell in another portion of the body. Different regions of the nephron bear specialized cells that have receptors to respond to chemical messengers and hormones. (Figure) summarizes the hormones that control the osmoregulatory functions.

Hormones That Affect Osmoregulation
Hormone Where produced Function
Epinephrine and Norepinephrine Adrenal medulla Can decrease kidney function temporarily by vasoconstriction
Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen
Angiotensin Liver Angiotensin II affects multiple processes and increases blood pressure
Aldosterone Adrenal cortex Prevents loss of sodium and water
Anti-diuretic hormone (vasopressin) Hypothalamus (stored in the posterior pituitary) Prevents water loss
Atrial natriuretic peptide Heart atrium Decreases blood pressure by acting as a vasodilator and increasing glomerular filtration rate decreases sodium reabsorption in kidneys

Epinephrine and Norepinephrine

Epinephrine and norepinephrine are released by the adrenal medulla and nervous system respectively. They are the flight/fight hormones that are released when the body is under extreme stress. During stress, much of the body’s energy is used to combat imminent danger. Kidney function is halted temporarily by epinephrine and norepinephrine. These hormones function by acting directly on the smooth muscles of blood vessels to constrict them. Once the afferent arterioles are constricted, blood flow into the nephrons stops. These hormones go one step further and trigger the renin-angiotensin-aldosterone system.

Renin-Angiotensin-Aldosterone

The renin-angiotensin-aldosterone system, illustrated in (Figure) proceeds through several steps to produce angiotensin II , which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I . Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).


Mineralocorticoids

Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. Aldosterone is a mineralocorticoid that regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. Because sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels but also the water levels in body fluids. In contrast, the aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. In contrast, absence of aldosterone means that no sodium gets reabsorbed in the renal tubules and all of it gets excreted in the urine. In addition, the daily dietary potassium load is not secreted and the retention of K + can cause a dangerous increase in plasma K + concentration. Patients who have Addison’s disease have a failing adrenal cortex and cannot produce aldosterone. They lose sodium in their urine constantly, and if the supply is not replenished, the consequences can be fatal.

Antidiurectic Hormone

As previously discussed, antidiuretic hormone or ADH (also called vasopressin ), as the name suggests, helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus and is stored and released from the posterior pituitary. It acts by inserting aquaporins in the collecting ducts and promotes reabsorption of water. ADH also acts as a vasoconstrictor and increases blood pressure during hemorrhaging.

Atrial Natriuretic Peptide Hormone

The atrial natriuretic peptide (ANP) lowers blood pressure by acting as a vasodilator . It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release, and because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.

Section Summary

Hormonal cues help the kidneys synchronize the osmotic needs of the body. Hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate the needs of the body as well as the communication between the different organ systems.


Osmoregulators and Osmoconformers

Persons lost at sea without any fresh water to drink are at risk of severe dehydration because the human body cannot adapt to drinking seawater, which is hypertonic in comparison to body fluids. Organisms such as goldfish that can tolerate only a relatively narrow range of salinity are referred to as stenohaline. About 90 percent of all bony fish are restricted to either freshwater or seawater. They are incapable of osmotic regulation in the opposite environment. It is possible, however, for a few fishes like salmon to spend part of their life in fresh water and part in sea water.

Organisms like the salmon and molly that can tolerate a relatively wide range of salinity are referred to as euryhaline organisms. This is possible because some fish have evolved osmoregulatory mechanisms to survive in all kinds of aquatic environments. When they live in fresh water, their bodies tend to take up water because the environment is relatively hypotonic, as illustrated in figure (a) below. In such hypotonic environments, these fish do not drink much water. Instead, they pass a lot of very dilute urine, and they achieve electrolyte balance by active transport of salts through the gills. When they move to a hypertonic marine environment, these fish start drinking sea water they excrete the excess salts through their gills and their urine, as illustrated in figure (b) below.

Most marine invertebrates, on the other hand, may be isotonic with sea water (osmoconformers). Their body fluid concentrations conform to changes in seawater concentration. Cartilaginous fishes’ salt composition of the blood is similar to bony fishes however, the blood of sharks contains the organic compounds urea and trimethylamine oxide (TMAO). This does not mean that their electrolyte composition is similar to that of sea water. They achieve isotonicity with the sea by storing large concentrations of urea. These animals that secrete urea are called ureotelic animals. TMAO stabilizes proteins in the presence of high urea levels, preventing the disruption of peptide bonds that would occur in other animals exposed to similar levels of urea. Sharks are cartilaginous fish with a rectal gland to secrete salt and assist in osmoregulation.

Fish are osmoregulators, but must use different mechanisms to survive in (a) freshwater or (b) saltwater environments. (credit: modification of work by Duane Raver, NOAA)

Career Connection: Dialysis Technician

Dialysis is a medical process of removing wastes and excess water from the blood by diffusion and ultrafiltration. When kidney function fails, dialysis must be done to artificially rid the body of wastes. This is a vital process to keep patients alive. In some cases, the patients undergo artificial dialysis until they are eligible for a kidney transplant. In others who are not candidates for kidney transplants, dialysis is a life-long necessity.

Dialysis technicians typically work in hospitals and clinics. While some roles in this field include equipment development and maintenance, most dialysis technicians work in direct patient care. Their on-the-job duties, which typically occur under the direct supervision of a registered nurse, focus on providing dialysis treatments. This can include reviewing patient history and current condition, assessing and responding to patient needs before and during treatment, and monitoring the dialysis process. Treatment may include taking and reporting a patient’s vital signs and preparing solutions and equipment to ensure accurate and sterile procedures.


41.5: Hormonal Control of Osmoregulatory Functions - Biology

C2006/F2402 '10 OUTLINE OF LECTURE #22

(c) 2010 Dr. Deborah Mowshowitz, Columbia University, New York, NY . Last update 04/21/2010 07:11 PM .

Handouts: 22A. Endocrine vs Exocrine Glands & catecholamines,

22B (Hormones Overall)
This topic is not covered in Becker. It is covered in Sadava/Purves. If you want a more detailed treatment, any physiology book will do. There are lots of good physiology books available the one by Sherwood & the one by Silverthorn have been used here for the last few years. There is an endocrinology book on line through Pubmed. Go to books to see the list of books available or to search by topic. Also don't forget about Kimball's biology pages.

I. Intro to Homeostasis, cont.

A. Regulation of Body Temperature (handout 21D ) -- See notes of last time.

B. The Circuit View (handout 21C ) -- See notes of last time.

II. Matching circuits and signaling -- an example: How the glucose circuit works at molecular/signaling level

Re-consider the circuit or seesaw diagram for homeostatic control of blood glucose levels -- what happens in the boxes on 21D? It may help to refer to the table below.

A. How do Effectors Take Up Glucose?

1. Major Effectors: Liver, skeletal muscle, adipose tissue

2. Overall: In response to insulin, effectors increase both uptake & utilization of glucose. Insulin triggers one or more of the following in the effectors:

a. Causes direct increase of glucose uptake by membrane transporters

b. Increases breakdown of glucose to provide energy

c. Increases conversion of glucose to 'stores'

(1). Glucose is converted to storage forms (fat, glycogen), AND

(2). Breakdown of storage fuel molecules (stores) is inhibited.

d. Causes indirect increase of glucose uptake by increasing phosphorylation of glucose to G-P, trapping it inside cells

3. How does Insulin Work?

a. Receptor: Insulin works through a special type of cell surface receptor, a tyrosine kinase linked receptor See Sadava 15.6. Insulin has many affects on cells and the mechanism of signal transduction is complex (activating multiple pathways). In many ways, insulin acts more like a typical growth factor than like a typical endocrine. (Insulin has GF-like effects on other cells is in same family as ILGFs = insulin like growth factors). More on GFs and TK receptors later.

b. How Does Insulin Increase Glucose Uptake in different effectors?

(1). In resting skeletal muscle & adipose tissue -- mobilizes GLUT 4:In these tissues insulin mobilizes transporter for facilitated diffusion (of glucose) -- GLUT 4 protein -- promotes fusion of vesicles containing the transporters with plasma membrane. No other hormone can cause this effect.

(2). In liver:Liver (& brain) can take up glucose without insulin -- they do not use GLUT 4. They use different transporters (GLUT 1, 2 &/or 3) located permanently in the plasma membrane.

(a). In liver: Insulin promotes glucose uptake in liver, but not directly. Insulin promotes uptake by increasing phosphorylation (trapping) and utilization of glucose.

(b). Note: Insulin has no affect on glucose uptake in brain.

(3). Working skeletal muscle:Insulin is not required for uptake of glucose in working skeletal muscle because exercise mobilizes GLUT4 in skeletal muscle. (Another good reason to exercise.)

c. Other Effects: In many tissues, insulin promotes utilization of glucose:

(1). Activates appropriate enzymes for synthesis of storage forms of metabolites -- synthesis of glycogen, fat, and/or protein.

(2). Inhibits enzymes for breakdown of stores.

(3). Can promote utilization (breakdown) of glucose for energy.

d. Significance: Some effects of insulin are mimicked by other hormones, but mobilization of GLUT4 cannot be triggered by any other hormone. Therefore loss of insulin, or lack of response to insulin, is very serious, and causes diabetes type I or II, respectively. (See absorptive state, below.)

B. How do Effectors Release Glucose?

1. Primary Effector for Release = Liver

a. Only organ that can release significant amounts of glucose into blood -- why? Liver has phosphatase for G-6-P. Muscle and adipose tissue don't.

b. Other tissues can breakdown stores (fat, glycogen) to release fatty acids or lactate into blood, but cannot release glucose.

2. Overall: Stores are broken down to generate small molecules liver releases glucose into blood.

  • Muscle has Epi receptors (but no glucagon receptors) therefore responds to Epi but not glucagon

  • Liver has receptors for both epi and glucagon and responds to both.

  • In muscle, breakdown to lactate, and release lactate to blood.

  • In liver, breakdown to glucose - P, and release glucose into blood.

d. Significance: Actions of glucagon can be mimicked by other hormones there is no known medical condition caused by lack of glucagon. (See post absorptive state below.)

C. Overall Function of Effectors -- Summary:

1. Liver -- both releases glucose to blood and stores excess (as glycogen).

a. Carries out both storage and release of glucose so acts as buffer.

b. Only organ that can release significant glucose into blood (kidney may do some).

c. Takes up glucose without insulin -- uses GLUT 2 (always in plasma membrane), not GLUT 4. Insulin stimulates phosphorylation & utilization of glucose, not direct uptake.

2. Muscle -- stores or releases energy.

Takes up glucose stores excess as glycogen.

When glycogen is broken down, releases lactate, not glucose, into blood.

3. Adipose Tissue -- stores or releases fat/ fatty acids.

Uses up glucose & fatty acids stores excess as fat.

When fat is broken down, releases fatty acids into the blood.

4. All three organs co-operate -- for example lactate generated in muscle is not broken down further in muscle -- it is shipped to liver and metabolized further in the liver. For many more details than you need see Sadava 50-20 (7th ed only) or advanced texts.

D. Absorptive vs Postabsorptive State -- A more complex view of the circuit

1. What is really being regulated by insulin & glucagon? Really two different things:

a. Maintenance of glucose homeostasis

b. Managing an episodic event (eating) -- this can be considered just another example of homeostasis -- here the 'episodic' nature of eating generates two basic states that must be controlled differently to maintain homeostasis.

2. There are two main states of food (not just glucose) supply. A detailed diagram of fuel traffic in both states (that goes way beyond what you need) is in Sadava fig. 50.20 (7th ed only) and in all physiology books.

a. Absorptive -- anabolic → synthesis & storage of macromolecules glucose is primary energy source. In this state, right after you eat, the risk is that blood glucose levels will rise too much. Absorptive state is completely dependent on insulin. Insulin affects all three effector organs.

b. Postabsorptive -- catabolic → breakdown of macromolecules to release glucose* fatty acids are primary energy source (except in brain). In this state, between meals, the risk is that blood glucose levels will falltoo much. Postabsorptive state is largely caused by lack of insulin also utilizes glucagon, but stress hormones (cortisol and epinephrine) can fill in for glucagon. Glucagon mainly affects liver.

*(Gluconeogenesis also occurs in liver = resynthesis of glucose from smaller molecules see texts if you are interested.)

For questions on this topic see problem set 7, questions 7-23 to 7-26, and 4R-3.

To review and to be sure you have this topic straight, fill in the following tables:

* Adipose tissue has glucagon receptors, but there is no known response to physiological levels of glucagon.

Insulin Glucagon
Type of Receptor/signaling pathway
Effect on blood glucose -- release or uptake?
Effect on glycogen -- synthesis or breakdown?
Result of intracellular glucose metabolism -- use it up or generate it?
Mobilize GLUT4?
Effect on pathways of intracellular glucose production -- inhibit or stimulate?


III. Introduction to Hormones (Endocrines) & Growth Factors

A. How to describe or classify hormones?

1. Many Possible Classification Schemes -- Hormones can be classified by effect, chemical nature, source (which gland?), target cells, etc. etc. See Topic V (for reference) for a extensive list.

2. Today: We will look at (1) processes controlled by hormones, (2) the major hormone producing glands, (3) details for specific hormones.

B. Summary of typical hormone roles and examples. See Becker Table 14-3 or Sadava fig. 41.5 (table 42.1) for a list of hormones by type of function (Becker) or by source (Sadava).

1. Stress response -- cortisol, epinephrine. Regulate heart rate, blood pressure, inflammation, etc.

2. Maintenance of Homeostasis -- insulin, glucagon. Regulate blood glucose/energy supplies and concentrations of substances in general. Maintain more or less constant conditions = homeostasis.

3. Regulation of episodic or cyclic events -- estrogen, insulin, oxytocin -- regulate lactation, pregnancy, effects of eating, etc.

4. Growth/overall regulation -- growth factors, tropic hormones -- regulate production of other hormones. (Note: not all GF's are endocrines.)

C. Overview of Major Glands & Hormones -- see handout 22B for overview. For a complete list see Sadava fig. 41.5 (Table 42.1)

  • When gland forms, epithelial layer leaves duct to outside.

  • Secretion from gland flows into duct → outside or lumen.

  • Examples:

When gland forms, epithelial layer pinches off leaving no duct

Secretion (hormone) from gland enters blood.

Example: gonads, pancreas, adrenal.

(3) Both types get precursors for secretions from blood

c. Regulation -- secretion of glucagon/insulin controlled by blood sugar levels and by input from sympathetic (in response to stress).

2. Adrenal Medulla & Cortex See Sadava fig. 41.11 (42.10).

a. Medulla (nervous)

(1). Stimulated by nerves

(2). Derived from neural tissue part of autonomic NS.

(3). Secretes compounds that can act as transmitters (when signal cell to cell) but act as hormones (neuroendocrines) here -- are released into the blood. Note same compound can act as a transmitter or a neuroendocrine.

(4). Major hormone = epinephrine (adrenaline) also secretes some norepinephrine (noradrenaline)For structures see handout 22A. More details below.

(5). Receptors. Receptors for these hormones/transmitters are same adrenergic receptors ( α & β) discussed previously.

(1). Stimulated by a hormone (ACTH)

(2). Derived from epithelial tissue

(3). Produces steroids = corticosteroids. For structures see Sadava fig. 41.12 (42.11).

(4). Part of HT/AP axis more details below or next time.

3. Additional info on dopamine (DA) & related compounds = catecholamines

  • Epinephrine acts mostly through beta adrenergic receptors.

  • Norepinephrine mostly through alpha adrenergic receptors.

  • activate adenyl cyclase

  • inhibit adenyl cyclase

  • activate phospholipase C.

See Previous lectures & problem 6-21 and 6-22 for examples of different responses to epi due to diff. receptors. For an example of the effects of dopamine, see problem 6-24.

4 . Hypothalamus (HT) -- neuroendocrine. HT is IC (integrative center) for many homeostatic circuits.

a. Inputs : 3 types of inputs

(1). neuronal

(2). hormonal

(3). local conditions. HT has sensors for some variables such as temperature, osmolarity.)

b. Outputs: To pituitary (also called hypophysis)

(1). To anterior pituitary (AP) also called adenohypophysis

(2). To posterior pituitary (PP) also called neurohypophysis

c. Details of structure and HT hormones below. (For structure, see handout 22B.)

5. Post. Pit. (Sadava fig. 41.6 (42.5).

a. Hormones = ADH = antidiuretic hormone (aka vasopressin) and oxytocin.

(1). ADH. Affects (primarily) water retention has 2 names because discovered twice from different effects. Details of action to be described when we get to kidney. (Works through IP3 or cAMP.)

(2). Oxytocin. Affects milk ejection, uterine contractions -- works (at least in part) through IP3 to affect Ca ++ and therefore contraction

b. Origin/action of hormones: Peptides are very similar in structure (homologous = share common evolutionary origin) but bind to different (G protein linked) receptors dif. effects.

6 . Anterior Pit -- Hypothalamus (HT) / Pituitary Axis

a. HT/Ant. Pit -- 3 stages

(1). HT → hormones (releasing factors) that signal the AP. Hormones go direct to AP through portal vessel (see handout 22B).

(2). AP (anterior pituitary) → tropic hormones (ACTH, LH, etc.) that signal to glands (endocrine tissue)

(3). Glands → lipid soluble hormones (steroids & TH) which control their target organs. Overall:

HTreleasing hormone AP tropic hormone TARGET GLAND hormone TARGET TISSUE action .

b. Example: How HT controls adrenal cortex

HTCRH AP ACTH ADRENAL CORTEX corticosteroids TARGET TISSUES action

(1). HT secretes corticotropin releasing hormone (CRH)

(2.) Ant. Pit responds by secreting ACTH (adrenal cortex tropic hormone also called adrenocorticotropin) into general circulation

(3). Adrenal cortex produces three major types of steroids = corticosteroids. For structures see Sadava 42.12 (41.11) .

(a). Glucocorticoids. Ex: cortisol -- involved in long term stress response (after epinephrine wears off) -- has multiple effects/targets, for ex. suppresses immune system. ACTH controls production of cortisol.

(b). Mineralocorticoids. Ex: aldosterone -- regulates salt balance (to be discussed when do kidney). Major control of aldosterone production is by other factors, not ACTH. ACTH has only a weak effect on aldosterone.

(c). Sex Steroids -- cortex produces low levels of sex hormones (both androgens and estrogens) in both sexes post puberty. That's how females get 'male' hormones and vice versa.

c. AP also → "other hormones" (GH, Prolactin, etc.) that signal to nonendocrine tissues.

7 . There are other glands/hormones -- the list so far is not exhaustive but covers most of the major players. See texts for complete lists.

It is worthwhile to memorize most of handout 22B in order to keep all the hormones and glands straight.

IV. Details of HT& Pituitary Set Up

A . Structure -- Two parts of pituitary (AP and PP) develop and function separately connected differently to HT.

  • Normally, blood flows from artery in general circulation → some tissue → vein in general circulation. Blood does not normally go direct from one organ to another.

  • Direct (Portal) vessel connects 2 organs.

b. Release: Hormones released from HT into the blood travel through portal vessel direct to AP.

c. AP is Epithelial. AP consists of epithelial tissue that grows up from mouth.

a. Cells connect HT & PP. Some cells of HT have bodies in HT and axons/terminals in posterior pituitary. (Sadava fig. 41.6 (42.5).

b. Release: Hormones (neuroendocrines) are released from nerve endings (terminals) in post. pit → general blood supply.

c. PP is neural. PP consists of neural tissue that grows down from brain.

B . Hypothalamic Hormones

1. Outputs (to AP): Some cells in HT release hormones from HT itself. (As vs. cells that connect to post. pit.)

a. Release hormones into portal vessel (see above) that goes direct to anterior pituitary.

b. Hormones are release factors. Hormones released by HT affect production/release of other hormones by ant. pit.

c. Affect on release -- 'release factors' can be stimulatory (RH's such as ACTH-releasing hormone) or inhibitory (IH's such as prolactin release-inhibiting hormone = PIH)

d. All HT hormones (except PIH = dopamine) are peptides/proteins.

2 . Outputs (to PP): Some cells in HT release hormones (ADH & oxytocin) from nerve endings in PP. Hormones are peptides made in cell body, packaged in vesicles, vesicles travel down MT's to end of neurons, hormones released by exocytosis.

V. How to Keep Track of Hormones -- How to Classify Hormones & Growth Factors (or Signal Molecules in General). The following is meant as a check list to help you keep track of the various signal molecules. It is for reference & study purposes it will not be discussed in class.
Some of these questions/categories overlap, and you can't answer all the questions for all the hormones, growth factors, etc., but the list helps to organize the information you do have.

1. Type of Action -- Is it paracrine, endocrine (hormone), growth factor, neurotransmitter, etc.? (See handout 12A)

2. Chemical nature -- Is it a peptide, amino acid or derivative, fatty acid or derivative, or steroid? See Becker table 14-4.

3. Where is it made? In what gland or tissue? (HT? pancreas?) See Sadava fig. 41.5 (Table 42.1)

4. Target Cells -- where does it act? (Muscle and liver? Just liver?)

5. Mechanism of signal transduction

A. Location/type of receptor on target cells -- Is receptor on surface or intracellular? TK* or G protein linked?

B. Type of signal transduction -- Is there a second messenger? Which one? If none, what links receptor to intracellular events?

C. Intracellular mode of action -- what mechanism is used to get the end result? Is there a change in enzyme activity? change in transcription? both? change in state of ion channel?

6. What actually gets done? What happens?

A. Biochemically speaking: Which target enzymes, proteins or genes are affected (glycogen phosphorylase activated? Gene for enzyme X transcribed?)

B. Physiological End Result: Another hormone secreted? Glycogen broken down, & Glucose in blood up? Note the "result" may have several steps, and more than one can sometimes be considered "the end."

C. What's the (teleological) point? What overall function is served by the signal molecule's action?

1. One list of possibilities: Homeostasis, response to stress, growth*, maintenance of some cycle

2. An alternative version of the list: Regulation of rates of processes, growth & specialization, Conc. of substances, and response to stress.

3. The 2 lists are really the same = homeostasis (control of rates & concentrations), response to stress, & regulation of growth (unidirectional and cyclic).

* Details of TK linked receptors have not been discussed (yet) in 2010. The point so far is that they are not GPCRs, and work differently.

Next Time: Details of HT/AP axis, examples of circuits using hormones & nerves, and signaling with TK receptors.


41.5: Hormonal Control of Osmoregulatory Functions - Biology

Download a printable version of this essay.

As you know, salmon spend most of their life in the open ocean, where they reach sexual maturity, but lay their eggs gravel beds at the upper reaches of (freshwater) streams. When the eggs hatch, the young salmon spend several months migrating downstream to the ocean where they remain for some 3-5 years. When mature, the adult salmon return to mouth of stream where they hatched (they remember the taste/smell of the water in the stream), migrate upstream to its headwaters, spawn, and die.
As you might expect, there are some serious physiological challenges presented by habitats as different as freshwater streams and the open ocean. The purpose of this essay is to discuss one of those challenges — how to keep the concentration and composition of their body fluids within homeostatic limits while migrating from fresh to salt water and back again — that salmon must cope with during their life cycle.

Osmoregulatory Problems for the Salmon
The information you need to know in order to understand salmon osmoregulation is presented in the following table.

Time course of the salmon's acclimation responses
The behavioral (drinking or not drinking) and physiological changes a salmon must make when moving from fresh water to salt water — and vice versa — are essential, but cannot be accomplished immediately. Thus, when a young salmon on its seaward journey first reaches the saline water at the mouth of its home stream, it remains there for a period of several days to weeks, gradually moving into saltier water as it acclimates. During this time, it begins drinking the water it's swimming in, its kidneys start producing a concentrated, low-volume urine, and the NaCl pumps in its gills literally reverse the direction that they move NaCl (so that they're now pumping NaCl out of the blood and into the surrounding water.
Likewise, when an adult salmon is ready to spawn and reaches the mouth of its home stream, it once again remains in the brackish ( = less concentrated than full-strength sea water) water zone of the stream's mouth until it is able to reverse the changes it made as a juvenile invading the ocean for the first time.


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Affiliations

Graduate Program in Organismic and Evolutionary Biology, University of Massachusetts, Amherst, MA, USA

Ciaran A. Shaughnessy & Stephen D. McCormick

Departamento de Biología, Universidad de Cádiz, Cádiz, Spain

Department of Biology, University of Massachusetts, Amherst, MA, USA

U.S. Geological Survey, Leetown Science Center, S.O. Conte Anadromous Fish Research Center, Turners Falls, MA, USA

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Contributions

C.A.S., A.B., and S.D.M. conceived of the project. C.A.S., A.B., and S.D.M conducted all live animal experimentation. C.A.S. performed molecular, radioimmunoassay, and receptor binding analyses. C.A.S. and A.B. performed enzyme activity analyses, data curation, and statistical analyses. C.A.S., A.B., and S.D.M. wrote and revised the original draft. S.D.M. was responsible for funding acquisition and project supervision.

Corresponding author


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