一氧化氮供体NOC 7可抑制去神经支配的NO耗竭兔肾中去甲肾上腺素和血管紧张素II诱导的肾反应。
A nitric oxide donor NOC 7 suppresses renal responses induced by norepinephrine and angiotensin II in the NO-depleted denevated rabbit kidney.
作者信息
Ono N, Adachi Y, Hashimoto K, Yoshida M, Suzuki-Kusaba M, Hisa H, Satoh S
机构信息
Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Aobayama, Sendai, Japan.
出版信息
Eur J Pharmacol. 1998 Jan 26;342(2-3):285-9. doi: 10.1016/s0014-2999(97)01565-3.
Intrarenal arterial infusion of norepinephrine (30 ng/kg per min) or of angiotensin II (4 ng/kg per min) reduced the glomerular filtration rate and urinary Na+ excretion in denervated kidneys of anesthetized rabbits pretreated intrarenally with a nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine methyl ester (50 microg/kg per min). Angiotensin II but not norepinephrine reduced fractional Na+ excretion. Intrarenal administration of a spontaneous NO donor 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC 7, 30 ng/kg per min) in L-NAME pretreated kidneys did not affect basal values, but attenuated the reduction in urinary Na+ excretion induced by these agonists without affecting the angiotensin II-induced reduction in glomerular filtration rate. The results suggest that NOC 7 can suppress the norepinephrine-induced hypofiltration and the angiotensin II-evoked tubular reabsorption and thereby attenuates the agonist-induced antinatriuresis in the denervated and endogenous NO-depleted rabbit kidney.
对麻醉兔的去神经支配肾脏预先经肾内给予一氧化氮（NO）合酶抑制剂N（ω）-硝基-L-精氨酸甲酯（50微克/千克每分钟），然后经肾内输注去甲肾上腺素（30纳克/千克每分钟）或血管紧张素II（4纳克/千克每分钟），会降低肾小球滤过率和尿钠排泄。血管紧张素II而非去甲肾上腺素会降低钠排泄分数。在预先用L-NAME处理的肾脏中经肾内给予自发NO供体1-羟基-2-氧代-3-（N-甲基-3-氨丙基）-3-甲基-1-三氮烯（NOC 7，30纳克/千克每分钟），对基础值无影响，但减弱了这些激动剂诱导的尿钠排泄减少，而不影响血管紧张素II诱导的肾小球滤过率降低。结果表明，NOC 7可抑制去甲肾上腺素诱导的滤过减少和血管紧张素II引起的肾小管重吸收，从而减弱激动剂诱导的去神经支配且内源性NO耗竭的兔肾脏中的抗利尿钠作用。
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