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We investigated the role of altered vascular calcium handling in the development of aldosterone-salt hypertension in the rat. The calcium sensitivity of isometric force in response to 50 mM KCl was compared in aortic rings from control and aldosterone-hypertensive rats. Over the entire range of calcium concentrations studied, responses in aortas from the hypertensives were significantly depressed compared to controls [ED50: aldosterone-hypertensive rats (n = 6), 0.739 +/- 0.137; controls (n = 7), 0.141 +/- 0.021 mM; P less than 0.001]. However, calcium sensitivity in response to 1 microM norepinephrine was similar in aortas from both hypertensives and controls [ED50: aldosterone-hypertensive rats (n = 7), 0.196 +/- 0.022; controls (n = 7), 0.180 +/- 0.024 mM]. The calcium sensitivity of Triton X-100 skinned aortic rings from aldosterone-hypertensive rats was likewise not significantly different from sensitivity in controls [ED50: aldosterone-hypertensive rats (n = 9), 3.61 X 10(-7) +/- 0.57; controls (n = 8), 3.89 X 10(-7) +/- 0.64 M]. Therefore, the observed decrease in calcium sensitivity in response to membrane depolarization in aortas from aldosterone-hypertensive rats probably is not due to a change in calcium sensitivity of the contractile system itself. The time course for development of changes in calcium handling in vessels from the aldosterone-hypertensive rats was found to be quite different from the time course for changes in monovalent ion metabolism. Whereas increases in monovalent ion permeability reportedly appear as early as one week after the start of aldosterone-salt treatment, significant alterations in calcium handling were not apparent until after four weeks of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium sensitivity of isometric force in intact and chemically skinned aortas during the development of aldosterone-salt hypertension in the rat.