Regulation of Vasopressin Release by Neurotransmitters, Neuropeptides and Osmotic Stimuli

Abstract

This chapter discusses the regulation of vasopressin (AVP) release from the neurohypophysis and the known effects of afferents to the supraoptic nucleus (SON). The signals regulating AVP release from the neurohypophysis for the maintenance of these functions involve osmoreceptive mechanisms located primarily in the hypothalamus and signals relayed from the cardiovascular volume and baroreceptors. AVP release is also altered by the changes in emotional states, pain, exercise, and the act of drinking. The AVP neurone itself is osmosensitive, in which increases in the osmolarity of the extracellular fluid cause depolarization of the membrane and a resulting sensitization of the neurone to other excitatory inputs. However, this inherent osmosensitivity is inadequate to generate firing of the neurone and subsequent AVP release by itself. The ability of osmotic stimulation to override noradrenergic inhibition emphasizes the prominent role of the osmotic control of AVP release and is consistent with the postulated role for the noradrenergic innervation in conveying signals from the cardiovascular baro- and volume-receptors. The interaction between noradrenaline and osmotic stimulation in determining AVP release would fit with a role for noradrenaline in transmitting cardiovascular information as the osmotic regulatory mechanisms can override the effects of noradrenaline. However, the information conveyed by the other chemically identified afferents to the SON remain to be established, and the mechanisms, which integrate all of these signals to achieve a rate of hormone release appropriate to the physiological circumstances, remain to be elucidated.