Figure 289

Neuroanatomy of the hypothalamus, where antidiuretic hormone (ADH) is synthesized, and the posterior pituitary gland, where ADH is released.

anteroventral region of the third ventricle, called the AV3V region. At the upper part of this region is a structure called the subfornical organ, and at the inferior part is another structure called the organum vas-culosum of the lamina terminalis. Between these two organs is the median preoptic nucleus, which has multiple nerve connections with the two organs as well as with the supraoptic nuclei and the blood pressure control centers in the medulla of the brain. Lesions of the AV3V region cause multiple deficits in the control of ADH secretion, thirst, sodium appetite, and blood pressure. Electrical stimulation of this region or stimulation by angiotensin II can alter ADH secretion, thirst, and sodium appetite.

In the vicinity of the AV3V region and the supraop-tic nuclei are neuronal cells that are excited by small increases in extracellular fluid osmolarity; hence, the term osmoreceptors has been used to describe these neurons. These cells send nerve signals to the supraop-tic nuclei to control their firing and secretion of ADH. It is also likely that they induce thirst in response to increased extracellular fluid osmolarity.

0 5 10 15 20 Per cent change

Figure 28-10

Both the subfornical organ and the organum vascu-losum of the lamina terminalis have vascular supplies that lack the typical blood-brain barrier that impedes the diffusion of most ions from the blood into the brain tissue. This makes it possible for ions and other solutes to cross between the blood and the local interstitial fluid in this region. As a result, the osmoreceptors rapidly respond to changes in osmolarity of the extracellular fluid, exerting powerful control over the secretion of ADH and over thirst, as discussed later.

Cardiovascular Reflex Stimulation of ADH Release by Decreased Arterial Pressure and/or Decreased Blood Volume

ADH release is also controlled by cardiovascular reflexes that respond to decreases in blood pressure and/or blood volume, including (1) the arterial barore-ceptor reflexes and (2) the cardiopulmonary reflexes, both of which are discussed in Chapter 18.These reflex pathways originate in high-pressure regions of the circulation, such as the aortic arch and carotid sinus, and in the low-pressure regions, especially in the cardiac atria. Afferent stimuli are carried by the vagus and glossopharyngeal nerves with synapses in the nuclei of the tractus solitarius. Projections from these nuclei relay signals to the hypothalamic nuclei that control ADH synthesis and secretion.

Thus, in addition to increased osmolarity, two other stimuli increase ADH secretion: (1) decreased arterial pressure and (2) decreased blood volume. Whenever blood pressure and blood volume are reduced, such as occurs during hemorrhage, increased ADH secretion causes increased fluid reabsorption by the kidneys, helping to restore blood pressure and blood volume toward normal.

Quantitative Importance of Cardiovascular Reflexes and Osmolarity in Stimulating ADH Secretion

As shown in Figure 28-10, either a decrease in effective blood volume or an increase in extracellular fluid osmolarity stimulates ADH secretion. However, ADH is considerably more sensitive to small changes in osmolarity than to similar changes in blood volume. For example, a change in plasma osmolarity of only 1 per cent is sufficient to increase ADH levels. By contrast, after blood loss, plasma ADH levels do not change appreciably until blood volume is reduced by about 10 per cent. With further decreases in blood volume, ADH levels rapidly increase. Thus, with severe decreases in blood volume, the cardiovascular reflexes play a major role in stimulating ADH secretion. The usual day-to-day regulation of ADH secretion during simple dehydration is effected mainly by changes in plasma osmolarity. Decreased blood volume, however,

The effect of increased plasma osmolarity or decreased blood volume on the level of plasma (P) antidiuretic hormone (ADH), also called arginine vasopressin (AVP). (Redrawn from Dunn FL, Brennan TJ, Nelson AE, Robertson GL: The role of blood osmo-lality and volume in regulating vasopressin secretion in the rat. J Clin Invest 52(12):3212, 1973. By copyright permission of the American Society of Clinical Investigation.)

Table 28-2

Regulation of ADH Secretion

Table 28-2

Regulation of ADH Secretion

Increase ADH

Decrease ADH

T Plasma osmolarity

0 Plasma osmolarity

0 Blood volume

T Blood volume

0 Blood pressure

T Blood pressure


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