Effects of Ganglionic and β-Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid 1

Summary

Arachidonic acid (AA) 300 μg/kg, and PGE₂, 5 μg/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF_2α, 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 PGF_2α 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 PGF_2α. Both PGE₂ and PGF_2α 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.