An analysis of some factors influencing alpha-adrenoceptor feed-back at the sympathetic junction in the rat heart.

Br J Pharmacol, 1979/5;66(1):55-63.

Docherty JR, McGrath JC

PMID: 222385

Impact factor: 9.473

Abstract
1 The effects of the selective prejunctional alpha-adrenoceptor antagonist, yohimbine, on the cardioacceleration responses to sympathetic stimulation were examined in the pithed rat. 2 Yohimbine reversed the inhibitory effects of the alpha-adrenoceptor agonist, clonidine, on the stimulation-induced tachycardia. 3 Yohimbine failed to potentiate significantly responses to stimulation in the absence of clonidine when stimulation was applied at the optimal level for cardiac responses (C6-T1). 4 When the pithing rod electrode was moved to T2-T6, cardioaccelerator responses were smaller and yohimbine produced potentiation at frequencies of greater than or equal to 1 Hz. This potentiation was prejunctional since responses to exogenous noradrenaline (NA) were not increased by yohimbine. 5 In the presence of cocaine, potentiation by yohimbine could be shown at the lower frequency of 0.1 Hz. 6 The possible physiological significance of a negative feed-back effect of noradrenaline on cardiac sympathetic nerves is discussed.
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