Effects of Ganglionic and -Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid

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Abstract
Summary Arachidonic acid (AA) 300 μg/kg, and PGE2, 5 μg/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF2α, 5 μg/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 PGF2α 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 μg/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 PGF2α. Both PGE2 and PGF2α have a direct positive inotropic effect on the heart. The persistent cardiac effects of PGE2 and PGF2 after β-adrenergic blockade suggests that these compounds may not interact with the β-receptors of the myocardium.

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