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  • Title: Positive inotropic response to alpha-adrenergic stimulation in an electrically driven rat left atrium: the role of extracellular calcium.
    Author: Shavit G, Gitter S, Barak Y, Vidne BA, Oron Y.
    Journal: J Cardiovasc Pharmacol; 1986; 8(2):324-31. PubMed ID: 2422471.
    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 increased and disappeared when external calcium concentration was raised to 7.0 mM. The divalent cation ionophore A23187 (1 microM) 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.
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