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Am J Physiol Regul Integr Comp Physiol 267: R1288-R1293, 1994;
0363-6119/94 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 5 1288-R1293, Copyright © 1994 by American Physiological Society

ARTICLES

Lack of increase in platelet Ca2+ and Na+ in deoxycorticosterone acetate-salt hypertensive rats

M. Ishida, T. Ishida, H. Matsuura, R. Ozono, G. Kajiyama and T. Oshima
First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.

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 mumol/l ionomycin in the Ca(2+)-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.


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