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心房利钠因子对急性单侧肾动脉狭窄犬肾素分泌、血浆肾素及醛固酮的影响。

Effect of atrial natriuretic factor on renin secretion, plasma renin and aldosterone in dogs with acute unilateral renal artery constriction.

作者信息

Sosa R E, Volpe M, Marion D N, Glorioso N, Laragh J H, Vaughan E D, Maack T, Atlas S A

机构信息

Cardiovascular Center, Cornell University Medical College, New Yor, NY 10021.

出版信息

J Hypertens Suppl. 1985 Dec;3(3):S299-302.

PMID:2856722
Abstract

Atrial natriuretic factor (ANF) decreases renin secretion rate (RSR), plasma renin activity (PRA) and plasma aldosterone (PA) in normal dogs. To clarify further the mechanisms responsible for these effects, the left renal artery was constricted in seven anaesthetized dogs prior to ANF administration. Constriction of the left renal artery decreased (P < 0.05) ipsilateral mean renal perfusion pressure (MRPP, 29 +/- 7%), renal plasma flow (RPF, 42 +/- 11%) and glomerular filtration rate (GFR) and filtered sodium load (FLNa, 21 +/- 8.8%). Ipsilateral RSR and peripheral PRA tended to increase, although not significantly. Atrial natriuretic factor infusion did not alter GFR in the clamped kidney and failed to decrease RSR or PRA. Despite this, PA levels decreased significantly (7.8 +/- 2.4 to 5.6 +/- 1.8 ng%). These results suggest that ANF-induced inhibition of renin secretion is largely consequent on its renal haemodynamic actions and that suppression of aldosterone by ANF in vivo is due, in part, to direct effects on the adrenal cortex.

摘要

心房利钠因子(ANF)可降低正常犬的肾素分泌率(RSR)、血浆肾素活性(PRA)和血浆醛固酮(PA)水平。为进一步阐明这些作用的机制,在给7只麻醉犬注射ANF之前,对其左肾动脉进行了缩窄。左肾动脉缩窄使同侧平均肾灌注压(MRPP,降低29±7%)、肾血浆流量(RPF,降低42±11%)、肾小球滤过率(GFR)和滤过钠负荷(FLNa,降低21±8.8%)均降低(P<0.05)。同侧RSR和外周PRA虽有升高趋势,但未达到显著水平。注射心房利钠因子并未改变夹闭肾脏的GFR,也未能降低RSR或PRA。尽管如此,PA水平显著降低(从7.8±2.4降至5.6±1.8 ng%)。这些结果表明,ANF诱导的肾素分泌抑制主要归因于其对肾脏血流动力学的作用,且ANF在体内对醛固酮的抑制作用部分是由于其对肾上腺皮质的直接作用。

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Effect of atrial natriuretic factor on renin secretion, plasma renin and aldosterone in dogs with acute unilateral renal artery constriction.心房利钠因子对急性单侧肾动脉狭窄犬肾素分泌、血浆肾素及醛固酮的影响。
J Hypertens Suppl. 1985 Dec;3(3):S299-302.
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