The effect of  -adrenoceptor and Ca2+ antagonist drugs on the hypoxia-induced increase in resting tension

Abstract

Using isolated, Langendorff-perfused, electrically-paced guinea-pig hearts, we have investigated the rise in resting tension that occurs when mammalian heart muscle becomes hypoxic. Substrate-depletion, tachycardia, hyperthyroidism, and inotropic interventions (ouabain, iso-prenaline, and β-receptor antagonists at concentrations which increase inotropic state) enhanced the rate of development of this increase in resting tension. 3.86 µmol·litre–1 propranolol, 0.22 to 2.20 µmol·litre–1 verapamil or removing Ca2+ from the extracellular phase at the <I>start</I> of the hypoxic episode prevented (or delayed) the rise in resting tension. Adding these same agents or removing Ca2+ from the extracellular phase <I>after</I> the hypoxia-induced rise in resting tension had started to develop failed to prevent its progression. These results provide some support for an hypothesis that the hypoxia-induced increase in resting tension is independent of an enhanced Ca2+ influx.