Presynaptic alpha receptors in relation to the cardiovascular effect of yohimbine in the anesthetized cat.

Yohimbine in doses of 0.1 and 0.5 mg/kg induced a prolonged graded elevation in mean arterial blood pressure (MABP) and pulse pressure (PP) in chloralose-anesthetized cats. However, an increased dose of yohimbine of 1.0 mg/kg resulted in a fall in blood pressure which lasted 30 min. All 3 dose levels produced an increase in heart rate (HR) but the response was maximal at 0.5 mg/kg. Therefore, further cardiovascular effects were investigated at this dose level. Propranolol pretreatment abolished yohimbine-induced tachycardia, but had little effect on the pressor response. Guanethidine pretreatment antagonized the tachycardia and converted the pressor response to yohimbine into a depressor one. Both tachycardia and rise in MABP obtained in response to yohimbine were abolished by hexamethonium pretreatment. In C-1 cord sectioned cats, only a transient tachycardia and rise in blood pressure were obtained. Yohimbine also augmented positive chronotropic response to the right cardioaccelerator nerve stimulation. Furthermore, yohimbine completely antagonized the inhibitory effect of clonidine on the positive chronotropic response induced by cardioaccelerator nerve stimulation. Therefore, a major fraction of the observed cardiovascular effects of yohimbine seems to be mediated indirectly via the released catecholamines secondary to the blockade by the drug, of presynaptic alpha adrenoceptors at sympathetic nerve terminals.