Renal and endocrine response to saline infusion in essential hypertension.
Renal and endocrine response to saline infusion in essential hypertension.
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原发性高血压患者对盐水输注的肾脏和内分泌反应。
DOI：
10.1161/01.hyp.8.3.217
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Hollenberg,NK
中科院分区：
文献类型：
--
作者：
Rydstedt,LL;Williams,GH;Hollenberg,NK
为了评估肾素-血管紧张素-醛固酮系统和肾脏血流动力学对原发性高血压患者急性肾钠处理的贡献，我们研究了21名原发性高血压患者（16名肾素正常，5名肾素低）和9名正常受试者。在接受小钠负荷（60meq， 1小时内静脉注射）之前，所有人的钠摄入量均为10meq，处于平衡状态。低肾素的高血压患者表现出预期的过度尿钠，这是一过性的，没有血压升高。肾素正常的高血压患者尿钠正常或迟钝；钠排泄延迟发生在一个亚群中，伴随着生理盐水负荷对肾素-血管紧张素-醛固酮系统的延迟抑制。在生理盐水负荷期间，肾脏血浆流量和肾小球滤过率均未发生变化。在用依那普利抑制转换酶72小时后，肾素反应迟钝的受试者的肾血浆流量显著增加，他们对钠负荷的利钠反应恢复正常。这些结果表明，当控制先前的钠摄入，避免大钠负荷，并将低肾素高血压作为一个混杂变量去除时，钝化而不是夸大的钠尿是原发性高血压的共同特征。这种异常可通过抑制血管紧张素转换酶逆转，这可能是由于转换酶抑制引起的肾血管舒张。
To assess the contribution of the renin-angiotensin-aldosterone system and renal hemodynamics to acute renal sodium handling in essential hypertension we studied 21 subjects who had essential hypertension (16 with normal renin, 5 with low renin) and 9 normal subjects. All were in balance on a 10 mEq sodium intake before receiving a small sodium load, 60 mEq intravenously over 1 hour. Hypertensive subjects with low renin showed the anticipated exaggerated natriuresis, which was transient and occurred without a rise in blood pressure. Natriuresis in hypertensive subjects with normal renin was either normal or blunted; delayed sodium excretion occurred in a subset, along with delayed suppression of the renin-angiotensin-aldosterone system by the saline load. Neither renal plasma flow nor glomerular filtration rate changed during the saline load. After 72 hours of converting enzyme inhibition with enalapril, renal plasma flow increased substantially more in the subjects with a blunted renin response and their natriuretic response to the sodium load returned to normal. These results indicate that when prior sodium intake is controlled, large sodium loads are avoided, and low renin hypertension is removed as a confounding variable, blunted rather than exaggerated natriuresis is the common feature of essential hypertension. This abnormality is reversed by angiotensin converting enzyme inhibition, perhaps because of converting enzyme inhibition-induced renal vasodilatation.