Susić H, Malik K U
J Pharmacol Exp Ther. 1981 Nov;219(2):377-82.
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.
研究了花生四烯酸对戊巴比妥麻醉犬在有无环氧化酶抑制剂甲氯芬那酸钠或吲哚美辛预处理情况下，由交感神经刺激、去甲肾上腺素和血管紧张素II引发的肾血管收缩反应的影响。以2至8赫兹的频率刺激肾神经，或将去甲肾上腺素或血管紧张素II（0.06 - 0.5微克）注入肾动脉，分别以频率和剂量相关的方式产生血管收缩并减少肾脏血流量。在未用环氧化酶抑制剂处理的动物中，以15微克/千克·分钟的速度肾动脉输注花生四烯酸可增加肾脏血流量，并减弱肾神经刺激、注入的去甲肾上腺素和血管紧张素II的血管收缩作用。然而，在预先用甲氯芬那酸钠或吲哚美辛（5毫克/千克）处理的犬中，输注花生四烯酸未能改变肾上腺素能刺激和血管紧张素II引发的肾血流量和血管收缩反应。相比之下，用环氧化酶抑制剂甲氯芬那酸钠预处理动物，并不妨碍前列腺素E2或前列环素（4纳克/千克·分钟）增加肾血流量并抑制肾上腺素能刺激或血管紧张素II产生的肾血管收缩反应。这些数据表明，花生四烯酸通过环氧化酶将其转化为一种或多种产物，可能是前列腺素E2和/或前列环素，从而产生肾血管舒张并减弱肾上腺素能刺激和血管紧张素II的血管收缩作用。
