Activation of α2-adrenoceptors attenuates the inotropic effect of field stimulation in atria

Abstract

Guinea-pig left atria were driven to contract at a rate of 0.5 Hz by stimulation with punctate electrodes. For additional field stimulation, a train of one to eight field pulses (30 V; 0.05–0.4 ms duration) was applied during each refractory period. Cholinergic effects were blocked by atropine and thus the resulting increase of the contractile force was caused by noradrenaline released from sympathetic nerve endings. Trains of several short field pulses delivered in the refractory period after each contraction produced a significantly greater inotropic effect than one single pulse of the same total duration delivered in each refractory period. Phentolamine, rauwolscine and idazoxan, by blocking prejunctional α 2-adrenoceptors selectively increased the inotropic effect of single field pulses. Selective blockers of α 1-adrenoceptors (prazosin, corynanthine) were ineffective in this respect. The effect of α 2-adrenoceptor blockers persisted in the presence of noradrenaline uptake blockers (cocaine or desipramine plus corticosterone) or phenylephrine, but was overcome by the α 2-adrenoceptor agonists, clonidine and guanabenz. It is concluded that activation of presynaptic α 2-adrenoceptors limits the release of noradrenaline by long-lasting single field pulses. Autoinhibition of transmitter release was not seen with trains of short field pulses.