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Alterations in vascular ionic metabolism preceded the onset of elevated blood pressure in the aldosterone-treated rat. Increases in 42K+ and 36Cl- turnover in the aorta and femoral artery were detected as early as 1 wk after the start of aldosterone infusion. These vascular changes were completely reversed after a 3-wk recovery period. An increased sensitivity to the effect of norepinephrine (NE) on aortic 42K+ turnover was also observed prior to a significant rise in systolic blood pressure. Enhanced sodium transport was also found in vessels from hypertensive rats infused with aldosterone for 4 wk. The potassium-sensitive component of the 24Na+ efflux was significantly elevated in vessels from hypertensives. This increase in sodium pump activity appeared to compensate for an increase in passive membrane permeability to sodium in that cell sodium levels were not altered by aldosterone treatment. A more rapid increase in 42K+ turnover occurred in aorta from aldosterone-treated rats when extracellular calcium was removed. Therefore, an impaired ability of calcium-dependent processes to adequately stabilize the vascular smooth muscle membrane may contribute to altered vascular ion transport. It is concluded that altered vascular electrolyte metabolism is an important pathogenic mechanism in the development of aldosterone-induced hypertension in the rat.
Garwitz et al. (Wed,) studied this question.