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灌注压变化和血管紧张素II对肾脏排泄心房利钠肽反应的影响。

The influence of changes in perfusion pressure and angiotensin II on the renal excretory responses to atrial natriuretic peptides.

作者信息

Chamienia A L, Johns E J

机构信息

Department of Physiology, Medical School, Birmingham, UK.

出版信息

Eur J Pharmacol. 1992 Aug 6;218(2-3):319-25. doi: 10.1016/0014-2999(92)90185-7.

Abstract

The renal actions of atriopeptin III were examined in anaesthetised rats at differing perfusion pressures before and following blockade of the renin-angiotensin system. At normal perfusion pressure 1000 ng kg-1 atriopeptin III caused reversible increases in glomerular filtration rate, of 20%, urine flow, absolute and fractional sodium excretions of 51-93%. Reduction of left renal perfusion pressure to 80 mm Hg decreased glomerular filtration rate by 30% and urine flow, absolute and fractional sodium excretions by 80% while atriopeptin III administration only minimally changed these variables. Concomitantly, right kidney perfusion pressure rose by 15 mm Hg which significantly increased fluid output, while the atriopeptin III induced diuresis and natriuresis were significantly larger. During infusion of captopril 900 micrograms kg-1 h-1 when pressures at the left and right kidneys had been reduced and elevated, respectively, atriopeptin III caused larger excretory responses in both kidneys which were greater than without captopril. These result suggested that the atriopeptin III mediated natriuresis and diuresis were directly proportional to perfusion pressure and attenuated by angiotensin II.

摘要

在阻断肾素-血管紧张素系统之前和之后,于不同灌注压力下对麻醉大鼠的心房肽III的肾脏作用进行了研究。在正常灌注压力下,1000 ng/kg的心房肽III可使肾小球滤过率可逆性增加20%,使尿流量、钠排泄绝对值和分数排泄率增加51%至93%。将左肾灌注压力降至80 mmHg可使肾小球滤过率降低30%,尿流量、钠排泄绝对值和分数排泄率降低80%,而给予心房肽III只会使这些变量发生微小变化。与此同时,右肾灌注压力升高15 mmHg,这显著增加了液体输出,而心房肽III诱导的利尿和利钠作用明显更大。在以900微克/千克·小时的速度输注卡托普利期间,当左肾和右肾的压力分别降低和升高时,心房肽III在两肾中均引起更大的排泄反应,且比未使用卡托普利时更大。这些结果表明,心房肽III介导的利钠和利尿作用与灌注压力成正比,并被血管紧张素II减弱。

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