Abstract
There is no longer any doubt about the presence of α-adrenoceptors in the heart of most mammalian species (10). In contrast to stimulation of s-adrenoceptors, that of α-adrenoceptors causes a positive inotropic but no chronotropic effect (10). Also in the anaesthetized intact cat, cardiac α-adrenoceptors have been demonstrated, stimulation of which also caused a positive inotropic effect — expressed as increase of left ventricular dp/dtmax — without increase in heart rate (12). The mechanism underlying stimulation of cardiac α-adrenoceptors is different from that of stimulation of s-adrenoceptors. Whereas stimulation of s-adrenoceptors is closely related to activation of myocardial adenylate cyclase (9) yielding to an elevation of cyclic AMP, that of α-adrenoceptors is not (2, 6, 7). Moreover, there is evidence that the positive inotropic effect induced by stimulation of α-adrenoceptors is strongly dependent on measures which influence the transsarcolemmal influx of Ca2+ as for instance organic calcium antagonists (3) as well as alteration of the extracellular calcium content or carbachol, for example (11). In isolated rabbit papillary muscle, these α-adrenoceptors have been found to be stimulated by the hormone adrenaline but not by the transmitter noradrenaline (4). This observation already has been obtained in the anaesthetized cat (12).
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