Yonago Acta medica 1992;35:105–116

Mechanisms of the Cardiovascular Effects of Centrally Administered Somatostatin in Rats

Masashi Watanabe

First Department of Internal Medicine, Faculty of Medicine, Tottori University, Yonago 683, Japan

To clarify the mechanisms of the cardiovascular response to intracerebroventricular (i.c.v.) administration of somatostatin (SRIF), the influence of pretreatment by i.c.v. α-antagonists or the intravenous (i.v.) administration of a vasopressin antagonist was investigated in pentobarbital-anesthetized male Wistar rats. Plasma arginine vasopressin (AVP) concentration was also measured. The i.c.v. SRIF (1.0 nmol/kg) caused an increase in mean arterial pressure (MAP) of 16 ± 2 mmHg and heart rate (HR) of 21 ± 3 beats/min, and an increase in plasma AVP concentration from 5.2 ± 0.7 to 21.7 ± 2.9 pg/mL (P < 0.05). Both pretreatment with i.c.v. phentolamine (200 µg/kg) and pretreatment with i.c.v. bunazosin (50 µg/kg) significantly attenuated the pressor response (16 ± 2 to 7 ± 2 mmHg, P < 0.05 or 16 ± 2 to 7 ± 1 mmHg, P < 0.05, respectively) and the plasma AVP response (21.7 ± 2.9 to 5.1 ± 1.6 pg/mL, P < 0.05 or 21.7 ± 2.9 to 6.7 ± 1.7 pg/mL, P < 0.05, respectively) to i.c.v. SRIF. Pretreatment with i.c.v. yohimbine (20 µg/kg) did not affect the cardiovascular responses to i.c.v. SRIF. Pretreatment with an intravenous administration of AVP antagonist significantly attenuated the pressor response to i.c.v. SRIF (16 ± 2 to 6 ± 1 mmHg, P < 0.05). These results suggest that the pressor response to i.c.v. SRIF is mediated through central α₁-adrenergic mechanisms which cause an elevation of plasma AVP concentration.

Key words: cardiovascular response; central α₁-adrenoceptors; intracerebroventricular administration; somatostatin; vasopressin

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