Attenuation by arachidonic acid of the effect of vasoconstrictor stimuli in the canine kidney.

The effect of arachidonic acid on the renal vasoconstrictor response elicited by sympathetic nerve stimulation, norepinephrine and angiotensin II in pentobarbital-anesthetized dogs, with and without pretreatment with the cyclooxygenase inhibitors, sodium meclofenamate or indomethacin was investigated. Stimulation of renal nerves at 2 to 8 Hz or injections into the renal artery of either norepinephrine or angiotensin II (0.06-0.5 micrograms) produced vasoconstriction and decreased blood flow to the kidney in frequency- and dose-related manners, respectively. In animals that were untreated with the cyclooxygenase inhibitors, renal arterial infusion of arachidonic acid at 15 micrograms kg-1 min-1 increased blood flow to the kidney and attenuated the vasoconstrictor effect of renal nerve stimulation, injected norepinephrine and angiotensin II. However, in dogs pretreated with either sodium meclofenamate or indomethacin (5 mg/kg), infusion of arachidonic acid failed to alter the renal blood flow and the vasoconstrictor response elicited by both adrenergic stimuli and by angiotensin II. In contrast, pretreatment of animals with the cyclooxygenase inhibitor, sodium meclofenamate, did not prevent either prostaglandin E2 or prostacyclin (4 ng kg-1 min-1) from increasing renal blood flow and inhibiting the renal vasoconstrictor response produced by either adrenergic stimuli or by angiotensin II. These data suggest that arachidonic acid produces renal vasodilation and attenuates the vasoconstrictor effect of the adrenergic stimuli and angiotensin II through its transformation by cyclooxygenase into one or more produced, presumably prostaglandin E2 and/or prostacyclin.