Baines A D, DeBold A J, Sonnenberg H
Can J Physiol Pharmacol. 1983 Dec;61(12):1462-6. doi: 10.1139/y83-208.
To examine the mechanisms underlying the natriuretic action of a partially purified extract of rat atria (AE) we injected the equivalent of one atrium into isolated perfused rat kidneys. Some kidneys received an infusion of angiotensin II at 0.5 ng/min throughout the experiment. In the absence of angiotensin AE had a variable effect on renal vascular resistance (RVR) but, in the presence of angiotensin II, AE consistently decreased RVR by 3% for 5 min followed by a slight increase. Inulin clearance and filtration fraction increased slightly but significantly. AE increased sodium, chloride, phosphate, and free water clearance but not potassium excretion. Ventricular extract had no effect on any of these variables. Furosemide (50-250 micrograms) increased sodium, chloride, and potassium but not phosphate or free water excretion. AE did not alter dopamine or norepinephrine excretion. We conclude that AE increases the glomerular filtration rate (GFR) and inhibits tubular reabsorption by mechanisms which differ, at least in part, from those affected by furosemide.
为了研究大鼠心房部分纯化提取物(AE)利钠作用的潜在机制,我们将相当于一个心房的提取物注入离体灌注的大鼠肾脏。部分肾脏在整个实验过程中以0.5 ng/分钟的速度输注血管紧张素II。在没有血管紧张素的情况下,AE对肾血管阻力(RVR)有不同的影响,但在有血管紧张素II存在时,AE可使RVR持续降低3%达5分钟,随后略有升高。菊粉清除率和滤过分数略有但显著增加。AE增加了钠、氯、磷酸盐和自由水清除率,但未增加钾排泄。心室提取物对这些变量均无影响。呋塞米(50 - 250微克)增加了钠、氯和钾的排泄,但未增加磷酸盐或自由水排泄。AE未改变多巴胺或去甲肾上腺素的排泄。我们得出结论,AE增加肾小球滤过率(GFR)并抑制肾小管重吸收,其机制至少部分不同于受呋塞米影响的机制。