Abstract

Stimulation of cardiac alpha1-adrenoceptors elicits a positive inotropic effect (PIE) in ventricular myocardium of most mammalian species, but not that of the dog. Stimulation of alpha1-adrenoceptors by phenylephrine did not affect the contractile force in isolated dog ventricular trabeculae under control conditions at 0.5 Hz at 37 degrees C. Phenylephrine, however, induced a definite PIE under experimental conditions at a low frequency (0.1 Hz) and low temperature (29 degrees C). Endothelin-1 and angiotensin II, the Gq protein-coupled receptors (GqPCR) of which are coupled to Gq protein-mediated stimulation of phosphoinositide (PI) hydrolysis as phenylephrine, did not affect the contractile force under control conditions either. But they did produce PIE at 0.1 Hz at 29 degrees C. These findings indicate that stimulation of receptors that are coupled to acceleration of PI hydrolysis has the potential to produce a PIE, but the expression of the effect of stimulation of GqPCR including alpha1-adrenoceptors is prevented at signaling processes that are susceptible for stimulation frequency and experimental temperature in dog ventricular myocardium.

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