Positive Inotropic Response to α-Adrenergic Stimulation in an Electrically Driven Rat Left Atrium: The Role of Extracellular Calcium

Publisher Website
Google Scholar
Abstract
We studied the positive inotropic response induced by .alpha.-adrenergic receptor stimulation in an electrically driven rat left atrium. .alpha.-Adrenergic stimulation resulted in a prolonged positive inotropic response that reached its maximum within 5-7 min. The kinetics of the onset of the positive inotropic response were different for pure .alpha.-adrenergic, pure-.beta.-adrenergic, and mixed adrenergic stimulation. The positive inotropic responses to .alpha.- and .beta.-adrenergic agonists were not additive. The relative inotropic response to .alpha.-adrenergic stimulation decreased when external calcium concentration was raised to 7.0 mM. The divalent cation ionophore A23187 (1 .mu.M) produced a threefold increase of the contractility of the atrial preparation at 1.0 mM extracellular calcium, and no further .alpha.-adrenergic response was observed in its presence. Calcium channel antagonists verapamil and nifedipine markedly inhibited the response to .alpha.-adrenergic stimulation, with little effect on the .beta.-adrenergic stimulation, at a calcium concentration of 0.5 mM. The inhibitory effect of calcium channel antagonists could be fully reversed by increasing the extracellular calcium concentration. Our data suggest that the .alpha.-adrenergic contractile response in the rat atrium involves the mobilization of extracellular calcium through verapamil-sensitive calcium channels in a mechanism different from that for the .beta.-adrenergic response.