Effects of ganglionic and beta-adrenergic blockade on cardiovascular responses to the bisenoic prostaglandins and their precursor arachidonic acid.

Arachidonic acid (AA) 300 mug/kg, and PGE2, 5 mug/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF2alpha, 5 mug/kg, produced a pressor response. All three compounds increased myocardial contractile force, but the magnitude of the change following AA was less prominent. After ganglionic blockade, the depressor response to AA and PGE2 persisted and the pressor response to PGF2alpha was augmented. Myocardial contractile force did not increase following AA in ganglion-blocked animals indicating that the cardiac responses observed before hexamethonium were mediated by the baroreceptor reflexes. A much larger dose of AA (900 mug/kg) resulted in a small positive inotropic effect on the heart. This possibly represents a direct cardiac effect of AA, or may be indicative of increased biosynthesis of an intermediate endoperoxide, or PGE2 and PGF2alpha. Both PGE2 and PGF2alpha have a direct positive inotropic effect on the heart. The persist cardiac effects of PGE2 and PGF2 after beta-adrenergic blockade suggests that these compounds may not interact with the beta-receptors of the myocardium.