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H2-histaminergic activity of clonidine in the guinea pig heart.

Clonidine perfusion (1 muM) or injection (9.4 to 150.4 nmoles) into the isolated perfused guinea pig heart caused an increase in contractile force, phosphorylase a and cyclic adenosine monophosphate (cyclic AMP) levels. The effects of clonidine were blocked by burimamide (30 muM). Proranolol (1 muM), phentolamine (1 muM) or reserpine treatment (5 mg/kg i.p., 24 hours prior to the experiment) did not influence the cardiac effects of clonidine. Clonidine (0.1 - 100 muM) also produced a dose dependent positive inotropic effect on right ventricle strips but had a negative chronotropic effect on the spontaneously beating right atria at higher concentration (0.1 to 1.0 M). Burimamide did not block the clonidine-induced negative chronotropic effect. Clonidine did not increase contractile force in guinea pig left atria. It also did not influence the isoproterenol-and phenylephrine-induced increases in cardiac force of contraction but did antagonize the positive inotropic effect of 4-methylhistamine in the right ventricle. This observation suggests that clonidine may compete with 4-methylhistamine for the same receptor sites. The results indicate that the cardiac receptors for both biochemical and mechanical effects of clonidine are histamine receptors of the H2-type.