Abstract
Abstract
During the first 15 days of one-kidney, one-wrapped (1K1W) hypertension in rabbits, retention of sodium occurred compared with essentially normotensive 2K1W control rabbits (1K1W, 30 ± 9 meq/15 days vs 2K1W, −6 ± 15 meq/15 days, P < 0.02). Most of the sodium retention occurred between the fifth and eighth days of the hypertensive period (3.7 ± 0.9 meq/day vs control period, 0.8 ± 0.9 meq/day, P < 0.02). Sodium retention occurred even though sodium intakes were reduced (hypertensive period, 8.7 ± 1.0 meq/day vs control period, 16.3 ± 0.9 meq/day, P < 0.001), serum sodium and potassium levels remained normal, and no potassium retention occurred. Positive sodium balances of individual 1K1W rabbits for the first 8 days of the hypertensive period correlated directly with the degree of arterial necrosis and with the degree of cardiac enlargement (P < 0.05). Change in voluntary dietary sodium intake for the entire hypertensive period correlated directly with the elevation in blood pressure (δBP vs δNa intake, P < 0.01). Consequently, reduction in sodium excretion due to decreased intake moderated 1K1W hypertension (δBP vs δNa Ex, P < 0.01) but was not related to the degree of cardiovascular disease. This study indicates that in the induction of 1K1W hypertension: (1) sodium retention occurs in a setting of reduced sodium intake; (2) development of arterial disease appears to be related to mechanisms of sodium retention; whereas (3) elevation of blood pressure occurs after sodium retention has occurred and is related to the total sodium intake and excretion.
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