Okahara T, Abe Y, Imanishi M, Yukimura T, Yamamoto K
Am J Physiol. 1981 Jul;241(1):F77-84. doi: 10.1152/ajprenal.1981.241.1.F77.
Prostaglandin E2 (PGE2) concentration in arterial and renal venous plasma was determined by radioimmunoassay in anesthetized dogs, and the PGE2 secretion rate was calculated. Intrarenal arterial infusion of CaCl2 (0.68 meq/min) resulted in a biphasic effect on renal blood flow (RBF) and an initial increase followed by a gradual decrease below the preinfusion level. PGE2 secretion rate increased from 7.2 +/- 4.4 to 95 +/- 28 ng/min, with a marked increase of RBF after 3 min of CaCl2 infusion. An equivalent amount of NaCl infused into the renal artery did not affect either the RBF or the PGE2 secretion rate. One-tenth the dose of CaCl2 (0.068 meq/min) infused into the renal artery did not increase either RBF or PGE2 secretin rate, and the RBF gradually decreased after infusion. The transient renal vasodilation observed during infusion of a high dose of CaCl2 ceased with the combined intrarenal infusion of verapamil (100 micrograms/min), and was also abolished by pretreatment with indomethacin (5 mg/kg i.v.). Infusion of CaCl2 (0.68 meq/min) into the femoral artery did not enhance the PGE2 secretion rate from the hindlimb, and femoral blood flow decreased immediately after the infusion. These results suggest tht the renal vessels as well as other resistance vessels are essentially constricted by calcium and that endogenous PGE2 released by calcium may modify this renal vasoconstriction.
通过放射免疫分析法测定了麻醉犬动脉和肾静脉血浆中前列腺素E2(PGE2)的浓度,并计算了PGE2的分泌率。肾内动脉输注氯化钙(0.68毫当量/分钟)对肾血流量(RBF)产生双相效应,最初增加,随后逐渐下降至输注前水平以下。PGE2分泌率从7.2±4.4增加到95±28纳克/分钟,在输注氯化钙3分钟后肾血流量显著增加。向肾动脉输注等量的氯化钠对肾血流量或PGE2分泌率均无影响。向肾动脉输注十分之一剂量的氯化钙(0.068毫当量/分钟)既未增加肾血流量也未增加PGE2分泌率,输注后肾血流量逐渐下降。在高剂量氯化钙输注期间观察到的短暂肾血管舒张在联合肾内输注维拉帕米(100微克/分钟)时停止,并且也被吲哚美辛预处理(5毫克/千克静脉注射)消除。向股动脉输注氯化钙(0.68毫当量/分钟)并未提高后肢的PGE2分泌率,输注后股血流量立即下降。这些结果表明,肾血管以及其他阻力血管基本上受到钙的收缩作用,并且钙释放的内源性PGE2可能会改变这种肾血管收缩。