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Figure 28-8

Osmoreceptor-antidiuretic hormone (ADH) feedback mechanism for regulating extracellular fluid osmolarity in response to a water deficit.

Figure 28-8

Osmoreceptor-antidiuretic hormone (ADH) feedback mechanism for regulating extracellular fluid osmolarity in response to a water deficit.

these signals down the stalk of the pituitary gland to the posterior pituitary.

3. These action potentials conducted to the posterior pituitary stimulate the release of ADH, which is stored in secretory granules (or vesicles) in the nerve endings.

4. ADH enters the blood stream and is transported to the kidneys, where it increases the water permeability of the late distal tubules, cortical collecting tubules, and medullary collecting ducts.

5. The increased water permeability in the distal nephron segments causes increased water reabsorption and excretion of a small volume of concentrated urine.

Thus, water is conserved in the body while sodium and other solutes continue to be excreted in the urine. This causes dilution of the solutes in the extracellular fluid, thereby correcting the initial excessively concentrated extracellular fluid.

The opposite sequence of events occurs when the extracellular fluid becomes too dilute (hypo-osmotic). For example, with excess water ingestion and a decrease in extracellular fluid osmolarity, less ADH is formed, the renal tubules decrease their permeability for water, less water is reabsorbed, and a large volume of dilute urine is formed. This in turn concentrates the body fluids and returns plasma osmolarity toward normal.

ADH Synthesis in Supraoptic and Paraventricular Nuclei of the Hypothalamus and ADH Release from the Posterior Pituitary

Figure 28-9 shows the neuroanatomy of the hypothalamus and the pituitary gland, where ADH is synthesized and released. The hypothalamus contains two types of magnocellular (large) neurons that synthesize ADH in the supraoptic and paraventricular nuclei of the hypothalamus, about five sixths in the supraoptic nuclei and about one sixth in the paraventricular nuclei. Both of these nuclei have axonal extensions to the posterior pituitary. Once ADH is synthesized, it is transported down the axons of the neurons to their tips, terminating in the posterior pituitary gland. When the supraoptic and paraventricular nuclei are stimulated by increased osmolarity or other factors, nerve impulses pass down these nerve endings, changing their membrane permeability and increasing calcium entry. ADH stored in the secretory granules (also called vesicles) of the nerve endings is released in response to increased calcium entry. The released ADH is then carried away in the capillary blood of the posterior pituitary into the systemic circulation.

Secretion of ADH in response to an osmotic stimulus is rapid, so that plasma ADH levels can increase severalfold within minutes, thereby providing a rapid means for altering renal excretion of water.

A second neuronal area important in controlling osmolarity and ADH secretion is located along the

Pituitary

Osmoreceptors

Supraoptic neuron

Anterior lobe \

Pituitary

Osmoreceptors

Supraoptic neuron

Anterior lobe \

■ Baroreceptors Cardiopulmonary receptors

■ Paraventricular neuron

Posterior lobe

Posterior lobe

■ Baroreceptors Cardiopulmonary receptors

■ Paraventricular neuron

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