Volpe M, Odell G, Kleinert H D, Müller F, Camargo M J, Laragh J H, Maack T, Vaughan E D, Atlas S A
Hypertension. 1985 May-Jun;7(3 Pt 2):I43-8. doi: 10.1161/01.hyp.7.3_pt_2.i43.
We previously provided evidence that atrial natriuretic factor (ANF) antagonizes angiotensin II-induced vascular contractility and angiotensin II-stimulated aldosterone production by isolated adrenal cells. To examine the importance of these effects in vivo, synthetic ANF (auriculin A) was administered intravenously (2 micrograms/kg bolus followed by 0.3 microgram/kg/min constant infusion) to conscious, unrestrained two-kidney, one-clip and one-kidney, one-clip rats on normal sodium intake and their sham-operated controls. The one-kidney, one-clip rats also were studied on a sodium-deficient diet. Mean blood pressure, plasma renin activity, and plasma aldosterone levels were measured before and after 60-minute infusion. In saralasin-responsive two-kidney, one-clip rats (n = 10), ANF administration reduced blood pressure (from 187 +/- 11 [SE] to 153 +/- 11 mm Hg; p less than 0.001) and plasma aldosterone levels (from 182 +/- 61 to 125 +/- 60 ng/dl; p less than 0.05), while plasma renin activity increased (from 59 +/- 16 to 82 +/- 20 ng/ml/hr; p less than 0.05). Lesser changes in blood pressure occurred in saralasin-nonresponsive two-kidney, one-clip rats (149 +/- 10 to 143 +/- 8 mm Hg; n = 5), sodium-replete one-kidney, one-clip rats (183 +/- 9 to 170 +/- 11 mm Hg; n = 9), two-kidney sham-operated rats (122 +/- 3 to 115 +/- 4 mm Hg; n = 8), and one-kidney sham-operated rats (117 +/- 3 to 112 +/- 3 mm Hg; n = 7). Control plasma renin and aldosterone levels were not elevated in these latter groups and did not change significantly with ANF administration. In sodium-depleted one-kidney, one-clip rats, which became saralasin responsive, ANF administration significantly reduced blood pressure (from 184 +/- 11 to 156 +/- 12 mm Hg; n = 8), plasma aldosterone levels (from 286 +/- 41 to 179 +/- 36 ng/dl), and plasma renin activity (from 69 +/- 19 to 44 +/- 13 ng/ml/hr).(ABSTRACT TRUNCATED AT 250 WORDS)
我们之前提供的证据表明,心房利钠因子(ANF)可拮抗血管紧张素II诱导的血管收缩以及血管紧张素II刺激离体肾上腺细胞产生醛固酮。为了研究这些作用在体内的重要性,将合成的ANF(耳状素A)静脉注射给正常钠摄入的清醒、未束缚的两肾一夹和一肾一夹大鼠及其假手术对照组(静脉推注2微克/千克,随后以0.3微克/千克/分钟持续输注)。一肾一夹大鼠也在低钠饮食条件下进行了研究。在输注60分钟前后测量平均血压、血浆肾素活性和血浆醛固酮水平。在对沙拉新有反应的两肾一夹大鼠(n = 10)中,给予ANF可降低血压(从187±11[标准误]降至153±11毫米汞柱;p<0.001)和血浆醛固酮水平(从182±61降至125±60纳克/分升;p<0.05),而血浆肾素活性增加(从59±16升至82±20纳克/毫升/小时;p<0.05)。在对沙拉新无反应的两肾一夹大鼠(149±10至143±8毫米汞柱;n = 5)、钠充足的一肾一夹大鼠(183±9至170±11毫米汞柱;n = 9)、两肾假手术大鼠(122±3至115±4毫米汞柱;n = 8)和一肾假手术大鼠(117±3至112±3毫米汞柱;n = 7)中,血压变化较小。后几组的对照血浆肾素和醛固酮水平未升高,给予ANF后也无显著变化。在变为对沙拉新有反应的低钠一肾一夹大鼠中,给予ANF可显著降低血压(从184±11降至156±12毫米汞柱;n = 8)、血浆醛固酮水平(从286±41降至179±36纳克/分升)和血浆肾素活性(从69±19降至44±13纳克/毫升/小时)。(摘要截断于250字)