Hormones of the posterior pituitary

• • Made up of distal neuron terminals

  • Secreted hormones; arginine vasopressin (ADH), oxytocin — both are peptide hormones.

  • Cell bodies located in the supraoptic nucleus and paraventricular nucleus of the hypothalamus.

Arginine vasopressin (ADH)

• • ADH is a major controller of water excretion and regulator of extracellular osmolarity.

  • The osmoreceptor neurons in the hypothalamus are extremely sensitive and are able to maintain ECF osmolarity within a very narrow range.

  • There is a downward shift in plasma osmolarity regulation in pregnancy, the menstrual cycle, and with volume depletion. In the latter case osmoregulation is secondary to volume regulation; a return of circulating volume occurs even though osmolarity decreases.

  • Volume receptors are less sensitive than osmoreceptors and a change of 10–15% in volume is required to produce a measurable change in ADH.

  • Angiotensin II and CRH can stimulate the release of ADH.

Synthesis and Release of ADH

• • ADH is synthesized in the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus; it is stored and released from the posterior pituitary.

  • Osmoreceptors are neurons that respond to increased plasma osmolarity, principally plasma sodium concentration. They synapse with neurons of the SO and PVN and stimulate them to secrete ADH from the posterior pituitary. They also stimulate consumption of water through hypothalamic centers that regulate thirst.

  • The SO and PVN also receive input from cardiopulmonary mechanoreceptors, as well as arterial baroreceptors. High blood volume or blood pressure tends to inhibit secretion of ADH.

  • Secretion of ADH is most sensitive to plasma osmolarity (1%); however, if blood volume decreases by 10% (such as hemorrhage) or cardiac output falls, high levels of ADH are secreted even if it causes abnormal plasma osmolarity.

  • ADH is also stimulated by Ang II and CRH.

Action of ADH

• • The main target tissue is the renal collecting duct (V2 receptors).

  • ADH increases the permeability of the duct to water by placing water channels (aquaporins) in the luminal membrane.

  • ADH, acting via the V1 receptor, contracts vascular smooth muscle.

Osmoregulation

• • An increase of only 1% in the osmolality of the ECF bathing the hypothalamic osmoreceptors evokes an increased in ADH secretion.

  • A similarly sized decrease in osmolality decreases ADH secretion.

  • In this manner, ECF osmolality is kept very close to 285 mOsm/Kg.

Volume Regulation

• • Stimuli arising from stretch receptors act to chronically inhibit ADH secretion.

  • Decreases in blood volume cause venous and arterial stretch receptors to send fewer signals to the CNS, decreasing chronic inhibition of ADH secretion.

  • This mechanism is especially important for restoring ECF volume following a hemorrhage.

Effect of Alcohol and Weightlessness on ADH Secretion

Ingesting ethyl alcohol or being in a weightless environment suppresses ADH secretion. In weightlessness, there is a net shi of blood from the limbs to the abdomen and chest. is results in greater stretch of the volume receptors in the large veins and atria, thus suppressing ADH secretion.

Atrial Natriuretic Peptide (ANP)

ANP is the hormone secreted by the heart. ANP is found throughout the heart but mainly in the right atrium. The stimuli that release ANP (two peptides are released) are:

• • Stretch, an action independent of nervous involvement

  • CHF and all fluid overload states

ANP increases sodium loss (natriuresis) and water loss by the kidney because of, in part, an increase in glomerular filtration rate due to:

• • ANP-mediated dilation of the afferent arteriole

  • ANP-mediated constriction of the efferent arteriole