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Plasma Bradykinin Levels and Urinary Kallikrein Excretion in Normal Renin Essential Hypertension^*

JAMES H. MERSEY, GORDON H. WILLIAMS, RODICA EMANUEL, ROBERT G. DLUHY, PATRICK Y. WONG and THOMAS J. MOORE

Endocrine-Hypertension Unit, Peter Bent Brigham Hospital, and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115; and the Division of Gastroenterology, Department of Medicine, Albany Medical College, Albany, New York 12208

Previous studies have documented subnormal urinary kallikrein excretion in patients with essential hypertension. Since recent evidence suggests that renal kallikrein can contribute to the circulating kinin pool, it could be hypothesized that decreased activity of the kallikrein-kinin vasodilatory system may contribute to the hypertensive process in these patients by decreasing systemic vasodilator activity. To test this possibility, urinary kallikrein excretion and plasma kinin levels were compared in 30 hypertensive and 21 normotensive subjects. Only subjects with essential hypertension and normal levels of PRA were included in this study; the hypertensive and normotensive groups were similar with regard to age, sex, and race distribution. Subjects were studied in balance on a diet containing 10 meq Na/100 meq K-day. PRA and kinin levels were measured by RIA and urinary kallikrein was measured by the N-P-tosyl-Larginine-methyl ester esterase method. As in previous studies, it was found that mean urinary kallikrein excretion was significantly lower in sodium-restricted hypertensive subjects compared to normotensive subjects (20.4 ± 2.4 vs. 30.8 ± 4.5 esterase units/24 h; P < 0.01). However, the supine kinin levels were similar in the two groups (hypertensive, 3.3 ± 0.3 ng/ml; normotensive, 3.7 ± 0.6 ng/ml), and their kinin increments in response to upright posture were also not significantly different (hypertensives, 1.0 ± 0.3 ng/ml; normotensives, 1.3 ± 0.3 ng/ml). In both normotensive and hypertensive subjects, plasma kinin levels paralleled PRA levels. Thus, these results document that patients with normal renin essential hypertension have kinin levels within the normal range even though their urinary kallikrein excretion is subnormal. Therefore, it is improbable that altered circulating levels of kinin contribute to the hypertension in these patients. If the decrease in kallikrein excretion is contributing to the hypertensive process, it is probably mediated locally by altering renal function. (J Clin Endocrinol Metab 48: 642, 1979)

^* This work was supported in part by NIH Grants 5-ROI-HL16821, 1-ROI-HL18882, 5-FR2-AM01629, 1-F32-HL05144, and HL-18624. The clinical studies were carried out in the Clinical Research Center of the Peter Bent Brigham Hospital and were supported by NIH Division of Research Resources Grant 5-MO1-RR00888.

Present address: Department of Medicine, Veterans Administration Hospital, Baltimore, Maryland.

Received August 16, 1978.

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