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Hypertension, Vol 11, 411-415, Copyright © 1988 by American Heart Association

ARTICLES

Plasma kinin concentration in deoxycorticosterone-salt hypertension

M Nakagawa and A Nasjletti
Department of Pharmacology, University of Tennessee, Memphis.

We investigated the status of circulating kinins in rats with severe hypertension caused by drinking 1% NaCl (saline) and treatment with deoxycorticosterone (DOC, 25 mg/kg/wk s.c.) for 5 weeks. Saline- drinking rats treated with DOC had a higher systolic blood pressure (210 +/- 4 mm Hg) than did rats without DOC treatment drinking water (138 +/- 3 mm Hg) or saline (141 +/- 3 mm Hg). The concentration of kinins in the inferior vena cava plasma of DOC-salt hypertensive rats did not differ from the venous plasma kinin concentration in normotensive rats drinking water or saline. In contrast, the arterial plasma kinin concentration in DOC-salt hypertensive rats (7.0 +/- 0.8 pg/ml) was lower (p less than 0.002) than that in water-drinking controls (14.0 +/- 2.2 pg/ml); it also was lower (p less than 0.005) in saline-drinking rats (8.1 +/- 0.9 pg/ml) than in water-drinking controls. Infusion of bradykinin (20 micrograms/kg/min i.v.) increased arterial plasma kinins in all the groups. Nonetheless, the arterial plasma kinin concentration achieved during bradykinin infusion in DOC- salt hypertensive (1590 +/- 130 pg/ml) and in saline-drinking rats (1540 +/- 100 pg/ml) was lower than that in water-drinking rats (2140 +/- 210 pg/ml). On the other hand, during infusion of the kininase II inhibitor captopril (80 micrograms/hr i.p.) for 3 days, neither DOC- salt hypertensive rats nor saline-drinking normotensive rats exhibited significant reduction of arterial plasma kinins relative to the level in water-drinking controls. These data indicate that high salt intake, irrespective of the level of blood pressure, causes the arterial plasma concentration of kinins to fall.(ABSTRACT TRUNCATED AT 250 WORDS)

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