ABNORMAL REGULATION OF CYTOSOLIC CALCIUM AND PH IN PLATELETS OF SABRARATS IN EARLY PHASES OF SALT HYPERTENSION DEVELOPMENT

platelet cytosolic free calcium concentration ([Ca2+](i)) and pH (pH(i )) have been reported to be altered in both human essential and rat sp ontaneous hypertension. The aim of our study was not only to search fo r the occurrence of such alterations in platelets of rats with salt-in duced hypertension but also to investigate whether these changes might precede blood pressure rise in this form of experimental hypertension . Using fluorescent probes fura-2 and BCECF, basal values and thrombin -induced changes of [Ca2+](i) and pH(i) were determined in platelets o f young hypertension-prone (SBH) and hypertension-resistant (SBN) Sabr a rats fed either low-salt (0.3% NaCl) or high-salt (4% NaCl) diets. U nder the conditions of low salt intake, basal [Ca2+](i) values were si milar in SBH and SBN rats, whereas pH(i) was significantly lower in SB H than in SBN animals. Thrombin induced smaller [Ca2+](i) elevation bu t greater pH(i) rise in SBH rats compared with SBN animals. The initia l rate of thrombin-induced Mn2+ entry, which reflects the opening of a particular subclass of thrombin-operated Ca2+ channels, was similar i n both strains. The moderate hypertension elicited in SBH rats by high salt intake was not associated with major alterations of basal [Ca2+] (i) or pH(i) values. High salt diet feeding did not influence [Ca2+](i ) and pH(i) responses to thrombin in either strain. In contrast, high salt intake reduced thrombin-induced Mn2+ entry in SBN but not in SBH rats. Basal platelet [Ca2+](i) values correlated positively with systo lic but not with diastolic blood pressure. This could be ascribed to a very close relationship of basal [Ca2+](i) values with pulse pressure . The abnormalities of [Ca2+](i) and pH(i) handling in platelets of Sa bra rats with salt-dependent genetic hypertension differ from those de scribed in essential hypertensive patients or rat strains with spontan eous forms of genetic hypertension. Our study also indicated that alte rations of platelet [Ca2+](i) do not precede blood pressure elevation in salt hypertension.