Vikse A, Sejersted O M, Kiil F
J Pharmacol Exp Ther. 1985 Jul;234(1):261-6.
To examine whether autoregulatory dilation of preglomerular vessels enhances prostaglandin (PG)E2 and renin release during arachidonic acid infusion, the ureter was occluded or the renal artery constricted in anesthetized dogs. Intrarenal arachidonic acid infusion (40 micrograms X kg-1 X min-1) increased PGE2 release by 41 +/- 17 pmol/min at control pressures and by 149 +/- 60 pmol/min during ureteral occlusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) increased PGE2 release by 149 +/- 60 pmol/min at control pressures, by 505 +/- 211 pmol/min during ureteral occlusion and by 581 +/- 201 pmol/min during renal arterial constriction. Thus, PGE2 release during arachidonic acid infusion was trebled by autoregulatory dilation. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renin release by 6 +/- 2 micrograms of angiotensin I per min at control pressures, by 25 +/- 9 micrograms of angiotensin I per min during renal arterial constriction and during ureteral occlusion by 16 +/- 4 micrograms of angiotensin I per min, which was not significantly higher than induced by the lower rate of infusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renal blood flow by 54 +/- 5% at control pressures but exerted no vasoactive effect during ureteral occlusion and renal arterial constriction. We conclude that autoregulatory dilation enhances the stimulatory effects of arachidonic acid on renal PG synthesis. Both increased intrarenal PG concentration and autoregulatory dilation may contribute to enhancement of renin release. The stimulatory effects of arachidonic acid on PG synthesis and renin release are independent of the vasoactive effects of arachidonic acid.
为了研究在输注花生四烯酸期间,肾小球前血管的自身调节性扩张是否会增强前列腺素(PG)E2和肾素的释放,对麻醉犬进行输尿管阻塞或肾动脉缩窄。在对照压力下,肾内输注花生四烯酸(40微克×千克-1×分钟-1)使PGE2释放增加41±17皮摩尔/分钟,输尿管阻塞期间增加149±60皮摩尔/分钟。输注花生四烯酸(160微克×千克-1×分钟-1)在对照压力下使PGE2释放增加149±60皮摩尔/分钟,输尿管阻塞期间增加505±211皮摩尔/分钟,肾动脉缩窄期间增加581±201皮摩尔/分钟。因此,在输注花生四烯酸期间,PGE2的释放因自身调节性扩张而增加了两倍。输注花生四烯酸(160微克×千克-1×分钟-1)在对照压力下使肾素释放增加6±2微克每分钟血管紧张素I,肾动脉缩窄期间增加25±9微克每分钟血管紧张素I,输尿管阻塞期间增加16±4微克每分钟血管紧张素I,这并不显著高于较低输注速率所诱导的水平。输注花生四烯酸(160微克×千克-1×分钟-1)在对照压力下使肾血流量增加54±5%,但在输尿管阻塞和肾动脉缩窄期间没有血管活性作用。我们得出结论,自身调节性扩张增强了花生四烯酸对肾脏PG合成的刺激作用。肾内PG浓度增加和自身调节性扩张都可能有助于肾素释放的增强。花生四烯酸对PG合成和肾素释放的刺激作用与花生四烯酸的血管活性作用无关。