Neural Control of Cardiovascular Function: Role of Osmosensation

Osmosenstion is a fundamental homeostatic process that controls the release of vasopressin (AVP). Hypothalamic neurons that make and release AVP are intrinsically osmosensitive and receive input from extrinsic osmoreceptors. This review examines the role of osmoreceptors in sodium-sensitive hypertension and how this important regulatory input interacts with non-osmotic systems such as angiotensin II to support hypertension. Sustained activation of AVP neurons by salt loading can lead to changes in chloride homeostasis that reduces or reverses the inhibitory effects of taurine or GABA. This would mitigate the inhibitory effects of hypoosmolality and baroreceptor stimulation. These changes have been observed in several models of hypertension. In sodium-dependent hypertension and salt loading, the intrinsic osmosensitivity of AVP neurons is amplified. Angiotensin II, which contributes to several models of hypertension, increases excitation from extrinsic osmoreceptors. Together, these observations suggest that changes in osmosensation may contribute to alterations in AVP release involved in the pathogenesis of salt-sensitive hypertension.