Thermal stimulation of vasopressin and oxytocin (VP/OT) release from explants of the hypothalamo‐neurohypophyseal system (HNS)

Abstract

Maintenance of a constant body temperature is essential in homeotherms. Since evaporative heat loss is necessary for preventing hyperthermia, integration of the mechanisms regulating water and thermal homeostasis is required. We used HNS explants from adult rats to study the impact of increases in temperature on stimulation of VP/OT release. Increasing the temperature from 37 to 39.5°C over 1 hr caused a dramatic increase in VP (850%) and OT (405% of basal) release (both p<0.001). Simultaneously exposing explants to a ramp increase in osmolality (25mOsm/2.6 hrs with mannitol) doubled the response to temperature alone (VP‐ 1780%; OT‐860% of basal). Thermal stimulation of VP/OT release was significantly attenuated by combined exposure to gadolinium (100μM), a non‐specific blocker of mechanosensitive channels, and capsazepine (10μM), a selective antagonist of TRPV1 channels, but not by capsazepine alone. This is consistent with other evidence that modified and capsazepine‐insensitive TRPV1 and TRPV4 channels participate in thermal regulation of VP/OT release. The gadolinium/capsazepine resistant response may reflect non‐specific thermal enhancement of metabolic processes. This is further supported by the thermal stimulus causing an increase in VP/OT release from isolated neural lobes similar to that retained by HNS explants in the presence of gadolinium/capsazepine. Supported by NIH RO1 NS‐27975