Adrenergic stimulation and blockade on inferior mesenteric arterial blood flow (Q) were measured in anesthetized rhesus monkeys. Control Q was 25 +/- 2 (mean +/- SE) ml/min; aortic and portal venous pressures were 121 +/- 5 and 6.5 +/- 1.0 mmHg. Calculated inferior mesenteric arterial resistance was 5.10 +/- 0.42 peripheral resistance units. Norepinephrine (N), 10(-3) to 1.0 microgram/kg intra-arterially, caused dose-dependent decreases in Q. Epinephrine (E) increased Q at 10(-3) microgram/kg in 60% of the animals studied and decreased Q at the higher doses (10(-2) to 1.0 microgram/kg). Isoproterenol (I) increased Q at all four doses studied. Ten-minute infusions of N and E (0.5 microgram x kg-1 x min-1) caused sustained decreases, and I caused sustained increases in Q. Autoregulatory escape was not observed. alpha-Adrenergic receptor blockade (phenoxybenzamine) attenuated the vasoconstrictor responses to N, but did not "reverse" the vasoconstrictor response to E (vasodilation). beta-adrenergic receptor blockade (propranolol) attenuated the vasodilator responses to I, but did not alter significantly the responses to E or N. These data indicate that in the monkey colonic circulation, alpha-adrenergic receptor stimulation causes vasoconstriction and beta-adrenergic receptor stimulation causes vasodilation.
Effect of Beta-Adrenergic Receptor Blockade on Racing Performance of Greyhounds with Normal and with Denervated Hearts
