Expression of Ca2+ transport genes in platelets and endothelial cells in hypertension

Altered Ca2+ handling is observed in different cells in essential hypertens ion. We investigated the expression of sarco(endo)plasmic reticulum Ca2+-AT Pase (SERCA) and inositol 1,4,5-trisphosphate receptor (IP3R) isoforms in p latelets and aortic endothelial cells (EC) isolated from spontaneously hype rtensive (SHR) and Wistar-Kyoto (WKY) rats by ratio reverse-transcriptase-p olymerase chain reaction (RT-PCR) analysis and Western blotting. SERCA2b an d SERCA3 were assessed at mRNA (EC and platelets) and at protein level (pla telets). IP(3)R1, IP(3)R2, and IP(3)R3 mRNAs were demonstrated in both cell types, but only IP(3)R1 and IP(3)R2 proteins were detected in platelets. C ompared with WKY, SHR EC and platelets showed higher SERCA3 and IP(3)R2 exp ression and lower IP(3)R1 expression. We then investigated the effect of li sinopril (20 mg . kg(-1) . d(-1); 10-week treatment of 4-week-old rats or 2 -week treatment of adult rats) and captopril (100 mg . kg(-1) . d(-1); 2-we ek treatment of adult rats). Consequently, expression patterns of SERCAs an d IP(3)Rs were significantly modified. Except for SERCAs mRNA in platelets, all differences between SHR and WKY disappeared. However, SERCA3 remained the predominant isoform. Both EC and platelets demonstrated a high equal ex pression of IP(3)R2 mRNA. IP(3)R1 was the predominant platelet protein isof orm, as it was in untreated WKY. mRNA was also isolated from pancreatic isl ets of WKY and SHR, but no effect of either rat strain or of lisinopril tre atment was observed on the expression of the studied genes. We hypothesize that the identical expression pattern of SERCAs and IP(3)Rs after treatment with ACE inhibitors represents a different nonhypertensive configuration, which, through changes in intracellular Ca2+ handling, improves endothelial and platelet dysfunction in SHR but has no effect in WKY.