高血压患者利尿剂降压与刺激肾素作用的关系。

G Leonetti, L Terzoli, C Sala, C Bianchini, L Sernesi, A Zanchetti
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引用次数: 33

摘要

1. 在31例原发性高血压患者中,通过在利尿剂氯噻酮治疗2周之前和结束时立即输注血管紧张素II拮抗剂萨拉拉西,对慢性利尿剂治疗刺激肾素的升压作用进行了评估。2. 在利尿剂治疗下,发现萨拉拉西素引起的血压变化与血浆肾素活性值相关,因此,在利尿剂轻度刺激肾素的患者中再次观察到小的升压反应,而在肾素明显升高的患者中出现明显的降压反应。3.另一方面,氯噻酮的降压作用与利尿剂治疗下血浆肾素活性值呈相反方向相关:在利尿剂治疗后肾素活性明显升高的患者中,血压几乎没有下降,有时甚至升高。4. 由此可见,慢性利尿剂刺激肾素释放可能是限制利尿剂降压作用的一个因素。
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Relationship between the hypotensive and renin-stimulating actions of diuretic therapy in hypertensive patients.

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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