Abstract
J. W. CONSTANTINE and W. K. McSHANE, Analysis of the cardiovascular effects of 2-(2,6-dichlorophenylamino) -2'imidazoline hydrochloride (Catapres), European J. Pharmacol. 4 (1968) 109–123. The nature of the blood pressure response (pressor followed by depressor) caused by intravenous administration of Catapres was analyzed in preparations ranging from isolated tissues to intact animal. Contractions of rabbit aorta and dog vein caused by Catapres are inhibited by α-adrenergic blockers. Catapres protects α-adrenergic receptors from blockade by phenoxybenzamine. It is concluded that the hypertensive effect of Catapres is due to sympathomimetic constriction of peripheral vasculature. Blood pressure and heart rate of dogs decreased following administration of Catapres into the vertebral artery at doses ineffective intravenously, indicating that hypotension and bradycardia are centrally mediated. The direct causes of hypotension depend upon the dose of Catapres. At low doses hypotension is des solely to reduction in peripheral resistance. Higher doses decrease peripheral resistance and cardiac output. Excessive doses lower cardiac output; peripheral resistance is not affected or increased. Catapres does not exaggerate postural hypotension in dogs or monkeys.
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