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[原发性醛固酮增多症及低肾素、正常肾素和高肾素型高血压患者的直肠电位差与血浆醛固酮]

[Rectal electrical potential difference and plasma aldosterone in hyperaldosteronism and low-, normal- and high-renin hypertension].

作者信息

Skrabal F, Mauser R

出版信息

Wien Klin Wochenschr. 1976 Dec 10;88(23):777-81.

PMID:1014711
Abstract

Rectal electrical potential difference (P.D.), plasma aldosterone and plasma renin activity were measured in 25 normal subjects, 80 patients with untreated essential hypertension, 4 patients with primary and 9 patients with secondary hyperaldosteronism. In normal subjects the rectal P.D. was 26 +/- 10 mV (+/- S.D.); in patients with hyperaldosteronism it was 51 +/- 7 mV. Plasma aldosterone and rectal P.D. were correlated significantly (r = 0.84, p less than 0.001) in these two groups combined. In 29% of patients with low-renin hypertension, in 9% of patients with normal-renin hypertension and in 3 out of 8 patients with high-renin hypertension, rectal P.D. was found to be elevated in the presence of normal plasma and urinary aldosterone and no correlation was observed between plasma aldosterone and rectal P.D. (r = --0.09, n.s.). In 3 out of 7 patients with low-renin hypertension and high rectal P.D., plasma and urinary aldosterone were consistently suppressed. Since patients with low renin and high rectal P.D. responded favourably to spironolactone therapy it is suggested that mineralocorticoids other than aldosterone may contribute to the pathogenesis of the hypertension in these cases. The aetiology of raised rectal P.D. in normal and high-renin hypertension is not clear, but both catecholamines and angiotensin II may be involved. The measurement of rectal P.D. alone is of limited value as a screening test for primary hyperaldosteronism in hypertensive patients, but combined with renin measurements it is a valuable tool for further investigation of patients with suspected mineralocorticoid excess syndromes, as well as for adjusting therapy with competitive aldosterone antagonists in patients with proven primary or secondary hyperaldosteronism.

摘要

对25名正常受试者、80例未经治疗的原发性高血压患者、4例原发性醛固酮增多症患者和9例继发性醛固酮增多症患者测量了直肠电位差(P.D.)、血浆醛固酮和血浆肾素活性。正常受试者的直肠P.D.为26±10mV(±标准差);醛固酮增多症患者为51±7mV。这两组患者的血浆醛固酮与直肠P.D.显著相关(r = 0.84,p<0.001)。在低肾素性高血压患者中,29%的患者、正常肾素性高血压患者中9%的患者以及8例高肾素性高血压患者中的3例,在血浆和尿醛固酮正常的情况下,直肠P.D.升高,且未观察到血浆醛固酮与直肠P.D.之间的相关性(r = -0.09,无统计学意义)。在7例低肾素性高血压且直肠P.D.高的患者中,有3例患者的血浆和尿醛固酮持续受到抑制。由于低肾素且直肠P.D.高的患者对螺内酯治疗反应良好,提示在这些病例中,除醛固酮外的盐皮质激素可能参与了高血压的发病机制。正常和高肾素性高血压患者直肠P.D.升高的病因尚不清楚,但儿茶酚胺和血管紧张素II可能都与之有关。单独测量直肠P.D.作为高血压患者原发性醛固酮增多症的筛查试验价值有限,但与肾素测量相结合,对于进一步调查疑似盐皮质激素过多综合征的患者以及调整已证实的原发性或继发性醛固酮增多症患者的竞争性醛固酮拮抗剂治疗来说,是一种有价值的工具。

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[Rectal electrical potential difference and plasma aldosterone in hyperaldosteronism and low-, normal- and high-renin hypertension].[原发性醛固酮增多症及低肾素、正常肾素和高肾素型高血压患者的直肠电位差与血浆醛固酮]
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The spironolactone, amiloride, losartan, and thiazide (SALT) double-blind crossover trial in patients with low-renin hypertension and elevated aldosterone-renin ratio.螺内酯、氨氯吡咪、氯沙坦与噻嗪类药物(SALT)对低肾素性高血压和醛固酮-肾素比值升高患者的双盲交叉试验。
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[Excess of mineralocorticoids in essential hypertension: clinical-diagnostic approach].[原发性高血压中盐皮质激素过多:临床诊断方法]
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Renin-angiotensin-aldosterone system in arterial hypertension.动脉高血压中的肾素-血管紧张素-醛固酮系统
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Primary aldosteronism, a common entity? the myth persists.原发性醛固酮增多症,一种常见病症?误解依然存在。
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[High prevalence of undiagnosed primary hyperaldosteronism among patients with essential hypertension].[原发性高血压患者中未诊断出的原发性醛固酮增多症的高患病率]
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Alterations of calcium metabolism and of parathyroid function in primary aldosteronism, and their reversal by spironolactone or by surgical removal of aldosterone-producing adenomas.原发性醛固酮增多症中钙代谢和甲状旁腺功能的改变,以及螺内酯或手术切除醛固酮分泌腺瘤对其的逆转作用。
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Abnormally sustained aldosterone secretion during salt loading in patients with various forms of benign hypertension; relation to plasma renin activity.各种类型良性高血压患者在盐负荷试验期间醛固酮分泌异常持续;与血浆肾素活性的关系。
J Clin Invest. 1970 Jul;49(7):1415-26. doi: 10.1172/JCI106359.
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Does aldosterone-to-renin ratio predict the antihypertensive effect of the aldosterone antagonist spironolactone?醛固酮与肾素比值能否预测醛固酮拮抗剂螺内酯的降压效果?
Am J Hypertens. 2005 Dec;18(12 Pt 1):1631-5. doi: 10.1016/j.amjhyper.2005.06.010.

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Klin Wochenschr. 1980 Mar 17;58(6):299-306. doi: 10.1007/BF01476572.