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

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, isoprenaline, and beta-receptor antagonists at concentrations which increase inotropic state) enhanced the rate of development of this increase in resting tension. 3.86 mumol.litre-1 propranolol, 0.22 to 2.20 mumol.litre-1 verapamil or removing Ca2+ from the extracellular phase at the start of the hypoxic episode prevented (or delayed) the rise in resting tension. Adding these same agents or removing Ca2+ from the extracellular phase after 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.