Modulation of adrenergic neuroeffector events in the renal vasculature: role of prostaglandins.

The major products of arachidonic acid metabolism in the kidney (PGE2, PGI2, PGF2 alpha) influence adrenergic neuroeffector events. PGE2 and PGI2 inhibit the vasoconstrictor responses elicited by sympathetic nerve stimulation and by injected norepinephrine in the rabbit and dog kidney. PGE2 also reduces release of the adrenergic transmitter from the rabbit kidney. In contrast, PGF2 alpha enhances adrenergically induced vasoconstriction. In the rabbit kidney, release of the adrenergic transmitter and the vasoconstrictor responses to nerve stimulation and to injected norepinephrine are enhanced by blockade of prostaglandin synthesis, and are reduced during stimulation of prostaglandin synthesis by either arachidonic acid or bradykinin. In contrast, in the rat kidney, adrenergically induced vasoconstriction is enhanced by PGE2, PGI2, and arachidonic acid and is reduced by prostaglandin synthesis inhibitors. This suggests major species differences in the modulatory action of prostaglandins at the adrenergic neuroeffector junction. This difference between rat and other species could be due to difference in prostaglandin receptors or in the events resulting from the interaction of prostaglandins with the receptors at the adrenergic neuroeffector junction.