The Role of α1-and α2-Adrenoceptors in Canine Systemic Capacitance Vessels 'A Study with Measurement of Mean Circulatory Pressure'

We investigated the presence of α-adrenoceptor subtypes in systemic capacitance vessels by examining the effects of α1-and α2-agonists or antagonists on the mean circulatory pressure (MCP). Dogs were anesthetized with pentobarbital, and after total spinal anesthesia, epinephrine was given intravenously to maintain mean blood pressure at about 80 mmHg. 1. With intravenous injection of phenylephrine (α1-agonist, 10 μg/kg, n = 7), and of BHT 920 (α2-agonist, 5 μg/kg, n = 7), MCP increased significantly from 9.8 ± 0.4 (mean ± SE) to 10.9 ±0.3 mmHg (+11.2%, p<0.01), and from 9.3 ± 0.4 to 10.3 ± 0.4 mmHg (+10.8%, p < 0.05), respectively. 2. Intravenous injection of prazosin (α1-antagonist, 150 μg/kg, n = 7) and of yohimbine (α2-antagonist, 30μg/kg, n = 7) decreased MCP significantly from 9.9 ± 0.4 to 8.2 ± 0.5 mmHg (-17.2%, p < 0.01), and from 9.8 ± 0.2 to 7.6 ± 0.3 mmHg ('22.4%, p < 0.01), respectively. 3. Intravenous injection of phenylephrine (10 μg/kg, n = 7) after pretreatment with prazosin (150 jug/kg) decreased MCP significantly from 9.5 ± 0.3 to 7.8±0.3mmHg ('17.9%, p<0.01). MCP decreased significantly from 9.9 ± 0.3 to 8.2 ± 0.3 mmHg ('17.2%, p<0.01) after intravenous injection of BHT 920 (5 μg/kg, n = 7) following pretreatment with yohimbine (30 μg/kg). These results suggest that the α1-and α2-adrenoceptor subtypes exist in systemic capacitance vessels, and that both play a mediating role in systemic venoconstriction induced by their agonists in areflex dogs.