Changes in body fluid osmolality can cause various symptoms, and the rate at which osmolality changes affects how well it is tolerated. Rapid changes (within hours) are less well tolerated compared to gradual changes (over days to weeks). In fact, individuals who experience changes in body fluid osmolality over a long period of time may not show any symptoms. This is because cells have the ability to either eliminate intracellular osmoles over time in response to hypoosmolality or generate new ones in response to hyperosmolality, which helps maintain stable cell volume in neurons.

Several nephron segments express a different AVP receptor (V2) that plays a role in regulating urine volume and osmolality. When plasma AVP levels are low, a large volume of dilute urine is excreted (diuresis). Conversely, when plasma AVP levels are high, a small volume of concentrated urine is excreted (antidiuresis). AVP is a small peptide consisting of 9 amino acids, with arginine at position 8. It is synthesized in neuroendocrine cells located in the supraoptic and paraventricular nuclei of the hypothalamus.

The synthesized hormone is packaged in granules and transported down the axon of the cell to be stored in nerve terminals in the neurohypophysis (posterior pituitary). Factors influencing the secretion of AVP by the posterior pituitary include the osmolality of body fluids and the volume and pressure of the vascular system. Other factors, such as nausea (stimulates) and atrial natriuretic peptide (inhibits), can also affect AVP secretion. Additionally, certain drugs, both prescription and nonprescription, can influence AVP secretion. For instance, nicotine stimulates secretion while ethanol inhibits it.

AVP, also known as antidiuretic hormone (ADH), acts through V1 receptors to cause contraction of vascular smooth muscle. AVP secretion can be regulated by the osmolality of body fluids (osmotic control) as well as nonosmotic factors such as volume and pressure of the vascular system. Neurons in the supraoptic and paraventricular nuclei of the hypothalamus synthesize either AVP or oxytocin, with AVP-secreting cells being more predominant in the supraoptic nucleus and oxytocin-secreting neurons primarily found in the paraventricular nucleus.

The hypothalamus and pituitary gland play a crucial role in AVP secretion, with afferent fibers from baroreceptors carried by the vagus and glossopharyngeal nerves. Osmoreceptors in the hypothalamus and supraoptic neurons are also involved in regulating AVP secretion. The vasomotor center in the medulla oblongata, cerebellum, and optic chiasm are part of the pathway for AVP secretion.
Symptoms associated with changes in body fluid osmolality vary depending on how quickly osmolality is changed. Rapid changes in osmolality (i.e., over hours) are less well tolerated than changes that occur more gradually (i.e., over days to weeks). Indeed, individuals who have developed alterations in their body fluid osmolality over an extended period of time may be entirely asymptomatic. This reflects the ability of cells over time to either eliminate intracellular osmoles, as occurs with hypoosmolality, or to generate new intracellular osmoles in response to hyperosmolality and thus minimize changes in cell volume of the neurons (see several nephron segments express a different AVP receptor (V2) that mediates the kidneys’ ability to regulate the volume and osmolality of urine. When plasma AVP levels are low, a large volume of urine is excreted (diuresis), and the urine osmolality is less than that of plasma (i.e., dilute).
When plasma levels of AVP are high, a small volume of urine is excreted (antidiuresis), and the urine osmolality is greater than that of plasma (i.e., concentrated).
AVP is a small peptide that is 9 amino acids in length (arginine is found at position 8). It is synthesized in neuroendocrine cells located within the supraoptic and paraventricular nuclei of the hypothalamus.
The synthesized hormone is packaged in granules that are transported down the axon of the cell and stored in nerve terminals located in the neurohypophysis (posterior pituitary). The anatomy of the hypothalamus and pituitary gland are shown in
Fig.
35.3
Secretion of AVP by the posterior pituitary can be influenced by several factors. The primary physiological regulators of AVP secretion are (1) the osmolality of body fluids (osmotic) and (2) the volume and pressure of the vascular system (hemodynamic, or nonosmotic). Other factors that can alter AVP secretion include nausea (stimulates), atrial
The human form of vasopressin is arginine vasopressin (AVP), which is also known as antidiuretic hormone (ADH). AVP, acting though V1 receptors, causes vascular smooth muscle contraction. As described subsequently, aDiuresis is the term used for excretion of a large volume of urine. This may reflect either excretion of a large volume of water (water diuresis), or excretion of a large amount of solute (solute diuresis). bNeurons within the supraoptic and paraventricular nuclei synthesize either AVP or the related peptide oxytocin. AVP-secreting cells predominate in the supraoptic nucleus, whereas oxytocin-secreting neurons are primarily found in the paraventricular nucleus.
626 SECTION7Berne & Levy Physiology • Fig. 35.3 Anatomy of the hypothalamus and pituitary gland (midsagittal section) depicting the pathways for AVP section. Also shown are pathways involved in regulating AVP secretion. Afferent fibers from the baroreceptors are carried in the vagus and glossopharyngeal nerves. The inset box illustrates an expanded view of the hypothalamus and pituitary gland. Vagus and glossopharyngeal nerves Vasomotor center (medulla oblongata) Cerebellum Baroreceptor input Pituitary Posterior lobe AVP Paraventricular neuronsOsmoreceptors Supraoptic neurons Optic chiasm Anterior lobe natriuretic peptide (inhibits), and angiotensin II (stimulates). A number of drugs, prescription and nonprescription, also affect AVP secretion. For example, nicotine stimulates secretion, whereas ethanol inhibits secretion.
Osmotic Control of AVP Secretion