Platelet cytosolic free Ca2+ concentration and plasma cholesterol in untreated hypertensives.

It has been proposed that plasma cholesterol, a major risk factor for atherosclerosis, may modify cellular Ca2+. In particular, higher membrane cholesterol contents induce higher Ca2+ influx and decrease the activity of the Ca2+ pumps. Cellular Ca2+ may also control the number of accessible low density lipoprotein receptors. We investigated the question of whether plasma cholesterol influences cellular Ca2+ metabolism, by analysing the cytosolic free Ca2+ concentration [( Ca2+]i) in unstimulated platelets from 61 untreated hypertensive patients [systolic and diastolic arterial pressure: 157 +/- 3/95 +/- 2 mmHg (mean +/- s.e.m.), respectively, age 41.8 +/- 1.7 years, body mass index 24.7 +/- 0.6 kg/m2]. The subjects' plasma total cholesterol (5.5 +/- 0.5 mmol/l) and platelet [Ca2+]i concentration (228 +/- 7 nmol/l) were positively correlated (r = 0.375, P less than 0.003). This correlation persisted at constant age, arterial pressure or body mass index. Platelet [Ca2+]i tended to increase with plasma low-density lipoprotein concentration (n = 21, P = 0.01), and to decrease with the ratio of high-density lipoprotein cholesterol to total cholesterol (n = 21, P = 0.08). The observation that in normocholesterolaemic hypertensive patients [Ca2+]i concentration in unstimulated platelets was correlated with plasma cholesterol suggests that cell activation may be modulated by membrane fluidity or that cholesterol metabolism is influenced by cell Ca2+.