Susić H, Nasjletti A, Malik K U
J Pharmacol Exp Ther. 1981 Jul;218(1):103-7.
In the dog anesthetized with pentobarbital, the effect of bradykinin on the lowering of renal blood flow produced by bolus injections of angiotensin II was studied. Injection into the renal artery of angiotensin II (0.06--0.50 microgram) caused vasoconstriction and decreased blood flow to the kidney in a dose-related manner. Renal arterial infusion of bradykinin (10 ng kg-1 min-1), prostaglandin (PG) E2 (4 ng kg-1 min-1) or PGI2 (4 ng kg-1 min-1) produced renal vasodilation and inhibited the vasoconstrictor effect of angiotensin II. However, renal arterial infusion of another vasodilatory peptide, substance P (2 ng kg-1 min-1), did not alter the effect of angiotensin II on the renal vasculature. Pretreatment of dogs with an inhibitor of PG synthesis, sodium meclofenamate (5 mg/kg), abolished the inhibitory effect of bradykinin on angiotensin II-induced renal vasoconstriction. In contrast, renal arterial infusion of either PGE2 or PGI2 was equally effective in reducing the renal vascular effect of angiotensin II in animals with and without meclofenamate pretreatment. These results suggest that bradykinin reduces the reactivity of the renal vasculature to angiotensin II by a mechanism dependent upon PG synthesis.
在戊巴比妥麻醉的犬中,研究了缓激肽对静脉注射血管紧张素II所引起的肾血流量降低的影响。向肾动脉注射血管紧张素II(0.06--0.50微克)可引起血管收缩,并使肾血流量呈剂量依赖性减少。肾动脉输注缓激肽(10纳克/千克/分钟)、前列腺素(PG)E2(4纳克/千克/分钟)或前列环素(PGI2)(4纳克/千克/分钟)可引起肾血管舒张,并抑制血管紧张素II的血管收缩作用。然而,肾动脉输注另一种血管舒张肽,P物质(2纳克/千克/分钟),并未改变血管紧张素II对肾血管系统的作用。用PG合成抑制剂甲氯芬那酸钠(5毫克/千克)预处理犬,可消除缓激肽对血管紧张素II诱导的肾血管收缩的抑制作用。相反,在有或没有甲氯芬那酸钠预处理的动物中,肾动脉输注PGE2或PGI2在降低血管紧张素II对肾血管的作用方面同样有效。这些结果表明,缓激肽通过一种依赖于PG合成的机制降低肾血管系统对血管紧张素II的反应性。