Endothelial cells from spontaneously hypertensive rats exhibit lower resting intracellular calcium and impaired stimulation-induced calcium increases, which may contribute to altered endothelial function in hypertension.
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Does not change hypertension management; hypothesis-generating for endothelial calcium dysregulation in animal models, with human relevance left open.
Using the fura-2 fluorescence technique, the hypothesis that calcium homeostasis may be altered in vascular endothelial cells of spontaneously hypertensive rats (SHR) was examined. Endothelial cells (EC) were isolated from rat tail arteries and subcultured for up to three passages. The resting intracellular calcium ion concentration ([Ca2+]i) in EC from tail arteries was found to be significantly lower in SHR than that in normotensive Wistar-Kyoto (WKY) rats. Bradykinin and endothelin induced a lesser increase in [Ca2+]i in both the peak increase and the total amount of calcium increase during a defined period of time in tail artery EC from SHR, compared with the respective EC from WKY rats. However, there was no significant difference in angiotensin II induced increase in [Ca2+]i in tail artery EC between SHR and WKY rats. It is suggested that a lower resting [Ca2+]i and a selectively impaired stimulation-induced increase in [Ca2+]i in EC may contribute to the altered endothelium function in spontaneously hypertensive rats.
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Wang et al. (1995) studied this question.
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