Anti -Diuretic Hormone| Vasopressin |Endocrinology

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AntiDiuretic Hormone|vasopressin |Endocrinology

 Keywords: What is anti-diuretic hormone. What are the main functions of ADH? What is vasopressin? Herring bodies|Magnocellular neurosecretory neurons |Prepropressophysin|Neurophysin II 

Table of contents

1.	Introduction
2.	Site of secretion
3.	Regulation of secretion
4.	Mechanism of secretion
5.	Functions

Introduction

In this article, we will learn about anti-diuretic hormones in detail, including the site of secretion, the regulation of its secretion, the mechanism of action, and more.

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Site of secretion

Magnocellular neurosecretory neurons of the supraoptic nucleus in the hypothalamus secrete anti-diuretic hormone (ADH).

This hormone is secreted as 'Prepropressophysin,' which contains ADH, Neurophysin II, and glycoprotein. Proteolytic cleavage of Prepropressophysin liberates Anti-diuretic hormone, Neurophysin II, and glycoprotein. Neurophysin II is a carrier protein. Anti-diuretic hormone passes down in the axon bound to Neurophysin II in the hypothalamic-hypophyseal tract to the posterior pituitary. It is stored in the Golgi apparatus as Herring bodies in the nerve terminals. When appropriate nerve impulses arrive at the nerve endings, The anti-diuretic hormone is released into the blood.

When pars nervosa is absent(a scarce condition), anti-diuretic hormone is released into the circulation from the hypothalamus.

What are Herring bodies?

Herring bodies are coarse, large granules containing the anti-diuretic hormone.

Neurophysin II is a carrier protein that carries the anti-diuretic hormone intraneuronal and is released into the circulation separately from the hormone.

 

Neurophysin II carries ADH

Neurophysin I carries Oxytocin.

 

 

The biological half-life is 16 to 20 minutes.

The liver and kidneys inactivate the hormone.

Mode of action

Anti-diuretic hormone acts via three types of receptors: V1A, V1B, and V2.

Regulation of Anti-diuretic hormone secretion:

Stimulant of secretion:

1. Hyperosmalilty

The normal osmolality of blood is 298-295 milliosmoles/Kg.(liter).

A slight change in the osmolality of blood causes a significant shift in ADH secretin.

Osmoreceptors are present in the Organum Vasculosam of the Lamina Terminalis (OVLT)Supra optic crest. When osmolality increases, osmoreceptors shrink. This shrinkage generates impulses that travel via the hypothalamic-hypophyseal tract to the posterior pituitary, releasing Anti-diuretic Hormone.

2. Hypovolemia

Due to any cause, hypovolemia is a potent stimulus for anti-diuretic hormone secretion and release. Reduction of blood volume without any change of osmolality of body fluids will increase ADH secretion.

Venous receptors are also known as baroreceptors. There are two types of baroreceptors:

1. Low-pressure baroreceptors are present in the left and right atrium, vena cava, and great pulmonary veins. They monitor the fullness of the vascular system.

2. High-pressure baroreceptors are located in the carotid sinus and aortic arch and monitor high pressure.

Any reduction in intrathoracic blood volume increases ADH secretion. On standing, more blood flows in the lower limb, decreasing left atrial pressure, increasing ADH secretion, conserving water, and increasing blood volume.

3. Pain, nausea, and vomiting

4. Stress, emotional and physical

5. Exercise

6. Certain drugs, like morphine, barbiturates, acetylcholine, and beta-adrenergic agonists, increase ADH secretion. Drugs exert direct positive effects on the supraoptic nucleus.

7. Decrease blood pressure

8. Decrease in blood pressure: Angiotensin II level. Angiotensin II acts on areas 3 and 4 of the subfornical organ (intercolumnar tubercle) to increase water intake.

9. Increased body temperature

10. Hypoglycemia.

11. Diseases like pneumonia, tuberculosis, meningitis, stroke. Cirrhosis of the liver and nephrosis.

Inhibitors of secretion:

1. Hyposmolality: decreased osmolality of extracellular fluid causes osmoreceptors to swell, reducing ADH secretion so that excess fluid is excreted through urine.

Factors that shrink osmoreceptors will increase ADH secretion. Fluid is retained in the body to maintain the osmolality of body fluids.

Factors that cause swelling of osmoreceptors will decrease ADH secretion, and more fluid is excreted to maintain the osmolality of body fluids.

2. An increase in extracellular fluid or blood volume will stretch volume or stretch receptors and send impulses via the vagus to the supraoptic nucleus to decrease ADH secretion.

3. Decrease temperature

4. Hormones like cortisol, thyroxin

5. Aterial natriuretic peptide (ANP).

6. Alcohol ingestion

7. Drugs, for example, atropine, caffeine, ethanol, and alpha-adrenergic agonists.

8. Sleep

9. Carbon dioxide inhalation

Mechanism of action

Anti-diuretic hormone acts via three types of receptors: V1A, V1B, and V2, on the outer surface of the cell membrane.

V2 receptors are on the outer layer of the 'Principal cells' on the side of the collecting ducts of nephrons.

ADH combines with V2 receptors and stimulates G protein to form GTP on the inner layer of the cell membrane. The GTP acts on the phospholipids of the inner layer of the cell membrane and initiates the formation of Cyclic AMP, which in turn stimulates Phosphokinase A.

Cyclic AMP is a primary cell metabolism regulator and converts inactive protein kinases to their active form.

Active protein kinases catalyze protein phosphorylation, thereby altering their formation and activities.

'Phosphokinase A' enters the cell nucleus and initiates transcription and translation to form a particular protein called Aquqporin II.

Now, Phosphokinase A causes the migration of Aquqporin II to the cell membrane towards the collecting duct, increasing the number of Aquqporin II. Water passes from the collecting duct to the principal cells through Aquqporin II.

These water molecules from the principal cells pass through Aquqporin III and IV to the interstitial spaces and enter the blood circulation. Aquqporin III and IV are present on the basolateral sides of the principal cells.

The water molecules in the blood circulation perform two functions: 1. They increase the blood volume and restore hypovolemia, and 2. They decrease hyperosmolality towards normal osmolality.

V1 receptors are present on the arterial endothelium.ADH combines with these receptors and activates Phospholipase C, which is present on the inner surface of the cell membrane. Phospholipase C catalyzes the hydrolysis of Phosphatidylinositol diphosphate, which is present on the inner side of the cell membrane.

Hydrolysis of Phosphatidylinositol diphosphate' yields two-second messengers: Inositol triphosphate(IP3) and diacylglycerol(DAG).

Inositol triphosphate(IP3) diffuses to the endoplasmic reticulum and leads to the release of Ca ions. Ca ions cause smooth muscle contraction and increase peripheral resistance, raising blood pressure. Therefore, ADH is also known as Vasopressin.

ADH with receptor V1A causes glycogenolysis in the liver.

ADH with V1B stimulates ACTH release from the anterior pituitary, controlling aldosterone secretion.

Functions of ADH:

1. Increase water absorption from the distal convoluted table, mainly from the collecting tubule.

2. Increases blood pressure by causing vasoconstriction, thus raising peripheral resistance.

3. Stimulates glycogenolysis in the liver.

4. Controls ACTH secretion from the anterior pituitary gland.

Hashtags: What is an anti-diuretic hormone. What are the main functions of ADH? What is vasopressin? Neurophysin II #Magnocellular neurosecretory neurons# Prepropressophysin 

Internal links:https://blog.totalphysiology.com/2021/02/glands-we-must-know.html

https://blog.totalphysiology.com/2024/09/pituitary-glandmaster-gland.html

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