LACK OF INCREASE IN PLATELET CA2+ AND NA+ IN DEOXYCORTICOSTERONE ACETATE SALT HYPERTENSIVE RATS

We have previously characterized abnormal Ca2+ handling in platelets of spontaneously hypertensive rats (SHRs). In this study, we investigated whether cellular Ca2+ metabolism and/or Na+ concentration is altered in platelets of deoxycorticosterone acetate-salt hypertensive rats (DOCA rats). The resting cytosolic Ca2+ concentration ([Ca2+](i)) in platelets was significantly lower in DOCA rats than controls (54.5 +/- 1.4 vs. 61.2 +/- 2.3 nmol/l). The amplitude of the [Ca2+](i) transient induced by thrombin was significantly increased in the absence, but not the presence, of external Ca2+ in DOCA rats compared with control rats. The [Ca2+](i) response to 5 mu mol/l ionomycin in the Ca2+-free buffer was greater in DOCA rats than in controls (546 +/- 23 vs. 470 +/- 18 nmol/l), indicating larger intracellular Ca2+ stores. The rate of recovery of [Ca2+](i) after the peak response to thrombin was decreased in DOCA rats (79% at 0.1 U/ml and 91% at 1.0 U/ml thrombin of control rats). Cytosolic Na+ concentration ([Na+](i)) in platelets was similar in DOCA and control rats. Altered Ca2+ levels are not correlated with [Na+](i) in this salt-sensitive hypertensive model. Therefore, an increased [Ca2+](i) is not an obligatory phenomenon in hypertension.