Dietary NaCl loading increases platelet Ca2+ discharge capacity in salt resistant essential hypertension.

To clarify the relationship between cellular Ca2+ handling and salt sensitivity, we evaluated cytosolic free Ca2+ ([Ca2+]i) in fura-2 loaded platelets isolated from 20 inpatients with essential hypertension. They were placed on a low sodium diet (50 mmol/day) for one week, followed by one week on a high sodium diet (340 mmol/day). They were classified into salt-sensitive (SS, n = 8) or salt-resistant (SR, n = 12) based on changes in the mean blood pressure. During the low salt diet, basal [Ca2+]i, thrombin-evoked maximal Ca2+ responses, irrespective of the presence of 1 mM extracellular Ca2+, and ionomycin-sensitive intracellular Ca2+ discharge capacity were similar in salt-sensitive and salt-resistant patients. Platelet basal [Ca2+]i were increased in both groups by salt loading (SS, from 22.0 +/- 1.3 to 27.2 +/- 1.9 nM, p < 0.01; SR, from 20.1 +/- 0.8 to 24.4 +/- 1.3 nM, p < 0.05). The thrombin-evoked maximal Ca2+ responses both in the presence and absence of extracellular Ca2+ were unchanged by high salt intake. The rate constant of decline in Ca2+ after the peak response to thrombin was larger in SR than that in SS during the high salt diet period (SS, 0.004 +/- 0.001 sec-1; SR, 0.043 +/- 0.014 sec-1, p < 0.05). The intracellular Ca2+ discharge capacity was increased by excessive salt intake in the salt-resistant patients but was unchanged in the salt-sensitive patients (SS, from 658.1 +/- 52.8 to 639.6 +/- 91.9 nM; SR, from 690.8 +/- 65.1 to 803.3 +/- 65.1 nM, p < 0.05). An increased intracellular Ca2+ discharge capacity may play, at least in part, a significant role in preventing the elevation of blood pressure after salt loading in salt-resistant patients with essential hypertension.