Adachi Y, Hashimoto K, Ono N, Yoshida M, Suzuki-Kusaba M, Hisa H, Satoh S
Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Sendai, Japan.
Eur J Pharmacol. 1997 Apr 18;324(2-3):223-6. doi: 10.1016/s0014-2999(97)10009-7.
Intrarenal arterial infusion of angiotensin II (4 ng/kg per min) reduced glomerular filtration rate and urinary Na+ excretion without affecting fractional Na+ excretion. Infusion of norepinephrine (30 ng/kg per min) reduced both urinary Na+ excretion and fractional Na+ excretion with a slight hypofiltration. The angiotensin II- and the norepinephrine-induced renal responses were suppressed during simultaneous infusion of a spontaneous nitric oxide donor 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl 1-triazene (NOC 7, 30 ng/kg per min) which itself had little influence on the renal parameters. The results suggest that in the rabbit kidney in vivo NOC 7 can interfere with the angiotensin II-induced hypofiltration and norepinephrine-evoked tubular reabsorption and thereby suppresses their antinatriuretic actions.
肾内动脉输注血管紧张素II(4纳克/千克每分钟)可降低肾小球滤过率和尿钠排泄,但不影响钠排泄分数。输注去甲肾上腺素(30纳克/千克每分钟)可降低尿钠排泄和钠排泄分数,并伴有轻微的滤过减少。在同时输注自发性一氧化氮供体1-羟基-2-氧代-3-(N-甲基-3-氨基丙基)-3-甲基-1-三氮烯(NOC 7,30纳克/千克每分钟)期间,血管紧张素II和去甲肾上腺素引起的肾脏反应受到抑制,而NOC 7本身对肾脏参数影响很小。结果表明,在兔体内肾脏中,NOC 7可干扰血管紧张素II引起的滤过减少和去甲肾上腺素诱发的肾小管重吸收,从而抑制它们的利钠作用。