Platelet cytosolic free
calcium concentration ([Ca2+]i) and pH (pHi) have been reported to be altered in both human essential and rat spontaneous
hypertension. The aim of our study was not only to search for the occurrence of such alterations in platelets of rats with
salt-induced
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 pHi were determined in platelets of young
hypertension-prone (SBH) and
hypertension-resistant (SBN) Sabra rats fed either low-
salt (0.3% NaCl) or high-
salt (4% NaCl) diets. Under the conditions of low
salt intake, basal [Ca2+]i values were similar in SBH and SBN rats, whereas pHi was significantly lower in SBH than in SBN animals.
Thrombin induced smaller [Ca2+]i elevation but greater pHi rise in SBH rats compared with SBN animals. The initial rate of
thrombin-induced Mn2+ entry, which reflects the opening of a particular subclass of
thrombin-operated Ca2+ channels, was similar in both strains. The moderate
hypertension elicited in SBH rats by high
salt intake was not associated with major alterations of basal [Ca2+]i or pHi values. High
salt diet feeding did not influence [Ca2+]i and pHi 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 systolic 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 pHi handling in platelets of Sabra rats with
salt-dependent genetic
hypertension differ from those described in essential hypertensive patients or rat strains with spontaneous forms of genetic
hypertension. Our study also indicated that alterations of platelet [Ca2+]i do not precede blood pressure elevation in
salt hypertension.