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衰老对血压正常者及原发性高血压患者尿激肽释放酶排泄的影响。

The effect of aging on urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension.

作者信息

Naka T, Ogihara T, Hata T, Maruyama A, Mikami H, Nakamaru M, Gotoh S, Masuo K, Ohde H, Iwanaga K, Kumahara Y

出版信息

J Clin Endocrinol Metab. 1981 May;52(5):1023-6. doi: 10.1210/jcem-52-5-1023.

Abstract

The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.

摘要

在54名年龄为11至88岁的正常受试者以及37名年龄为17至82岁的原发性高血压患者中,研究了衰老对尿激肽释放酶排泄量(UkalV)的影响。同时还测量了这些受试者的尿钠、钾和醛固酮排泄量(U(Ald)V)。正常受试者和高血压患者的尿钠和钾排泄量均未随衰老而发生显著变化。在正常受试者中,U(kal)V(r = 0.45;P < 0.001)和U(Ald)V(r = 0.58;P < 0.01)均随年龄增长而显著降低。U(kal)V与U(Ald)V呈正相关(r = 0.44;P < 0.001)。相比之下,高血压患者的U(Ald)V随年龄增长显著降低(r = -0.36;P < 0.05),但U(kal)V未出现与年龄相关的显著变化。在高血压患者中,未观察到U(kal)V与U(Ald)V之间存在显著相关性。在60岁以下的个体中,正常受试者和高血压患者的U(kal)V值无显著差异。60岁以上的高血压患者比同年龄组的正常受试者排泄更多的尿激肽释放酶(P < 0.05)。总之,正常受试者中U(kal)V随年龄增长而降低可能是由于肾素 - 血管紧张素 - 醛固酮系统活性降低所致。高血压患者中U(kal)V未出现与年龄相关的降低是否与原发性高血压的发病机制或病理生理学相关,仍有待阐明。

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