Central effects of somatostatin: pressor response, AVP release, and sympathoinhibition.

The effects of intracerebroventricular (icv) administration of somatostatin(1-14) (SS1-14) on mean arterial blood pressure (MAP), heart rate (HR), plasma arginine vasopressin (AVP) concentration, and splanchnic nerve activity (SpNA) were studied in conscious rats. In addition, the effects of peripheral alpha-adrenergic receptor blockade with prazosin, vasopressinergic V1-receptor blockade with [d(CH2)5Tyr(Me)]AVP, and chronic bilateral sinoaortic denervation (SAD) on central SS1-14-induced MAP, HR, and SpNA responses were investigated. SS1-14 icv elicited dose-dependent increases in MAP and plasma AVP concentration as well as decreases in HR and SpNA. Prazosin iv did not significantly affect SS1-14-induced pressor and bradycardic responses but augmented the decrease in SpNA. The V1-AVP receptor antagonist iv significantly attenuated the effects of SS1-14 icv on MAP, HR, and SpNA. Following SAD the pressor responses to SS1-14 icv were significantly enhanced and were associated with significantly smaller decreases in HR and SpNA. We conclude that central administration of SS1-14 causes a pressor response via release of AVP while at the same time inhibiting peripheral sympathetic outflow. Our results support the hypothesis that SS1-14 in the brain by its effects on AVP release and sympathetic outflow may participate in central cardiovascular regulation.