Role of Vasopressin and α1-Adrenergic Mechanism in the Cardiovascular Effects of Intracerebroventricular Administration of Somatostatin in Rats

To clarify the mechanisms of the cardiovascular responses to Intracerebroventricular administration (i.c.v.) of somatostatin=14 (SS-14), the effects of pretreatment by i.c.v. α-antagonists or intravenous administration (i.v.) of vasopressin antagonist were investigated in conscious male Wistar rats. Plasma arginine vasopressin (AVP) concentration was also measured. The i.c.v. SS-14 (1.0nmol/kg) caused an increase in mean arterial pressure (MAP) of 16±2mmHg and a decrease in heart rate (HR) of -20 ±3 beats/min, and an increase in plasma AVP concentration from 3.2±0.7 to 21.7±2.9pg/ml (p< 0.05). Pretreatment with either i.c.v. phentolamine (200μg/kg) or i.c.v. bunazosin (50μg/kg) significantly attenuated the pressor response (16±2 to 7±2mmHg, p<0.05, or 16±2 to 7±1mmHg, p<0.05, respectively) and the plasma AVP response (21.7±2.9 to 4.8±1.8pg/ml, p<0.05, or 21.7 ±2.9 to 5.2±2.0pg/ml, p<0.05, respectively) to i.c.v. SS-14. Pretreatment with i.c.v. yohimbine (20 μg/kg) did not affect the cardiovascular responses to i.c.v. SS-14. Pretreatment with i.v. AVP antagonist significantly attenuated the pressor response to i.c.v. SS-14 (16±2 to 6±1mmHg, p<0.05). These results suggest that the pressor response to i.c.v. SS-14 is mediated through activation of central α1-adrenergic mechanisms which cause elevation of plasma AVP concentration.(Hypertens Res 1993; 16: 91-96)