Determinants of Platelet Intracellular Free Calcium in Essential Hypertension and Effect of Stimulation by Arginine Vasopressin

The aim of this study was to determine platelet intracellular free calcium with respect to age, sex, race, and agonist stimulation in patients with essential hypertension compared with normotensive subjects. Intracellular free calcium was measured, using Fura-2-AM, in 42 normotensive and 52 patients with untreated essential hypertension. Of these, 22 pairs were age, sex, and race matched. The intracellular free calcium response to agonist stimulation was measured in the presence of 1 /zmol/L arginine vasopressin (AVP). Intracellular calcium was significantly raised in patients with hypertension in both the matched and unmatched groups with values (means ± SEM) in the matched group of 68.4 ± 2.6 n m o l / L for the hypertensives and 60.2 ± 2.1 n m o l / L for the normotensives (n = 22; Ρ < .02) and in the unmatched group of 63.3 ± 1 . 8 n m o l / L (n = 52) and 57.6 ± 1.4 n m o l / L (n = 42, Ρ < .02), respectively. There was no sex difference but intracellular calcium was significantly lower in black hypertensives compared with white hypertensives (P < .005). A significant correlation with blood pressure was only observed in the combined normotensive and hypertensive group (r = 0.23; Ρ = .030). There was no significant correlation with age in any group (even when excluding the black individuals), but in the hypertensive group there was a significant correlation with serum cholesterol (r = 0.34, Ρ = .02; η = 46) The intracellular calcium response to AVP was significantly reduced in the hypertensive subjects compared with the normotensives in the presence of 1 m m o l / L extracellular calcium with increases of 523.0 ± 62.1 n m o l / L and 271.0 ± 35.7 n m o l / L for normotensives and hypertensives, respectively (P < .001). A significant difference was also observed in the absence of extracellular calcium. The raised intracellular free calcium and the differences in response to AVP, as well as the association with cholesterol, clearly reinforces the hypothesis of defective cellular calcium handling in essential hypertension. Am J Hypertens 1993;6:209-216