Vascular kallikrein in deoxycorticosterone acetate-salt hypertensive rats

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Abstract

We determined the status of vascular kallikrein in rats with severe hypertension caused by treatment with deoxycorticosterone acetate (DOCA) and drinking of 1% Nad for 6 weeks. We assayed active and total kininogenase (kallikrein) activity in the perfusate and in arterial and venous tissue. DOCA-salt rats had higher systolic blood pressure at 6 weeks (214±5 mm Hg) than rats drinking tap water (135±4 mm Hg) or saline (145±8 mm Hg). Kininogenase in the perfusate (nanograms bradykinin per minute per kilogram body weight) increased significantly at 2 weeks, from 5.8±2.1 to 8.9±1.4 for active kallikrein and from 28.7±0.4 to 48.7±2.9 for total kallikrein. Total kallikrein returned to control values at 4 weeks, whereas it was significantly reduced at 6 weeks (20.9±0.7). Active kallikrein was significantly depressed at 4 and 6 weeks (1.08±0.1 and 0.85±0.1, respectively [ P P

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APA

Nolly, H., Carretero, O. A., Lama, M. C., Miatello, R., & Guillermo Scicli, A. (1994). Vascular kallikrein in deoxycorticosterone acetate-salt hypertensive rats. Hypertension, 23(1), I-185-I–188. https://doi.org/10.1161/01.hyp.23.1_suppl.i185

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