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激肽和血管紧张素II对乳头血流调节的影响。

Influence of kinins and angiotensin II on the regulation of papillary blood flow.

作者信息

Roman R J, Kaldunski M L, Scicli A G, Carretero O A

机构信息

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226.

出版信息

Am J Physiol. 1988 Oct;255(4 Pt 2):F690-8. doi: 10.1152/ajprenal.1988.255.4.F690.

DOI:10.1152/ajprenal.1988.255.4.F690
PMID:2845811
Abstract

The influence of kinins and angiotensin II on the regulation of renal cortical and papillary blood flow and sodium and water excretion was examined in rats. Superficial cortical and papillary blood flows were measured using a laser-Doppler flowmeter. Papillary blood flow increased 50% after enalaprilat (60 micrograms/kg) and phosphoramidon (5.5 micrograms.kg-1.min-1) were given along with 0.3 M sodium bicarbonate solution to inhibit degradation of kinins and enhance urinary kallikrein activity. Infusion of a kinin antagonist, D-Arg-Hyp-Thi-D-Phe-bradykinin (5 micrograms/min), returned papillary blood flow to control levels. Urine flow and sodium excretion increased after the administration of the kininase inhibitors and sodium bicarbonate, while glomerular filtration rate (GFR) and outer cortical blood flow were unaltered. The kinin antagonist did not alter sodium and water excretion in rats receiving the kininase inhibitors and bicarbonate. Administration of the kinin antagonist alone lowered papillary blood flow by 20%, without affecting outer cortical blood flow or GFR. Urine flow decreased and urine osmolality increased after the rats received the kinin antagonist, but sodium excretion remained unaltered. To assess the role of angiotensin II in the control of papillary blood flow, kinin receptors were blocked by infusion of an antagonist, and the effects of enalaprilat and saralasin were studied. Papillary blood flow increased after blockade of the angiotensin II system in rats receiving the kinin antagonist. These results indicate that the kallikrein-kinin and renin-angiotensin systems participate in the regulation of papillary blood flow.

摘要

在大鼠中研究了激肽和血管紧张素II对肾皮质和乳头血流以及钠和水排泄调节的影响。使用激光多普勒血流仪测量浅表皮质和乳头血流。在给予依那普利拉(60微克/千克)和磷酰胺(5.5微克·千克-1·分钟-1)以及0.3M碳酸氢钠溶液以抑制激肽降解并增强尿激肽释放酶活性后,乳头血流增加了50%。输注激肽拮抗剂D-Arg-Hyp-Thi-D-Phe-缓激肽(5微克/分钟)可使乳头血流恢复到对照水平。给予激肽酶抑制剂和碳酸氢钠后,尿流量和钠排泄增加,而肾小球滤过率(GFR)和外皮质血流未改变。激肽拮抗剂对接受激肽酶抑制剂和碳酸氢盐的大鼠的钠和水排泄没有影响。单独给予激肽拮抗剂可使乳头血流降低20%,而不影响外皮质血流或GFR。大鼠接受激肽拮抗剂后尿流量减少,尿渗透压增加,但钠排泄保持不变。为了评估血管紧张素II在控制乳头血流中的作用,通过输注拮抗剂阻断激肽受体,并研究了依那普利拉和沙拉新的作用。在接受激肽拮抗剂的大鼠中,阻断血管紧张素II系统后乳头血流增加。这些结果表明,激肽释放酶-激肽系统和肾素-血管紧张素系统参与了乳头血流的调节。

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