Susić H, Malik K U
J Pharmacol Exp Ther. 1981 Sep;218(3):588-92.
The effect of prostaglandin E2 (PGE2) and prostacyclin (PGI2) on the renal venous output of the adrenergic transmitter and on the renal vasoconstriction produced by sympathetic nerve stimulation and by norepinephrine was studied in pentobarbital-anesthetized dog. Renal arterial infusion of either PGE2 or PGI2 (4 ng kg-1 min-1) increased blood flow to the kidney and inhibited the vasoconstrictor response elicited by renal nerve stimulation (1-8 Hz) and by renal arterial injections of norepinephrine (0.006-0.5 microgram). However, during infusion of either PGE2 or PGI2, the renal venous output of norepinephrine caused by nerve stimulation was not altered. In contrast, substance P (2 ng kg-1 min-1), which also increased the blood flow to the kidney, did not affect the renal vasoconstrictor response elicited by either adrenergic stimulus. These results suggest that PGE2 and PGI2 reduce the vasoconstrictor effect of sympathetic nerve stimulation in the canine kidney by acting on the vascular smooth muscle.
在戊巴比妥麻醉的犬身上,研究了前列腺素E2(PGE2)和前列环素(PGI2)对肾静脉肾上腺素能递质输出以及对交感神经刺激和去甲肾上腺素所产生的肾血管收缩的影响。经肾动脉输注PGE2或PGI2(4纳克/千克/分钟)可增加肾血流量,并抑制由肾神经刺激(1 - 8赫兹)和肾动脉注射去甲肾上腺素(0.006 - 0.5微克)所引发的血管收缩反应。然而,在输注PGE2或PGI2期间,神经刺激引起的去甲肾上腺素肾静脉输出未发生改变。相比之下,P物质(2纳克/千克/分钟)虽然也增加了肾血流量,但并不影响由任何一种肾上腺素能刺激所引发的肾血管收缩反应。这些结果表明,PGE2和PGI2通过作用于血管平滑肌来降低犬肾交感神经刺激的血管收缩效应。