AJP - Heart and Circulatory Physiology, Vol 243, Issue 6 927-H933, Copyright © 1982 by American Physiological Society
Altered arterial ion transport and its reversal in aldosterone hypertensive rat
E. T. Garwitz and A. W. Jones
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.
