Abstract 640: Role Of Endothelial No Synthase Expression On Endothelial Dysfunction In Hypertensive Patients

Previous studies have implicated impairment in the expression of endothelial NO synthase (eNOS) and the S1177 phosphorylated form of eNOS in mediating endothelial dysfunction in the spontaneously hypertensive rats. However, the relevance of this observation in human hypertension remains unknown. Accordingly, we assessed endothelial function in 19 patients with untreated essential hypertension (HTN) and 18 age-matched normotensive controls (NT), using noninvasive flow mediated vasodilation (FMD) in the brachial artery. We also assessed endothelial cell (EC) protein expression of eNOS and S1177 phosphorylated eNOS using immunofluorescence staining of the ECs extracted via J wire insertion into antecubital veins. We found that FMD was significantly reduced in the HTN versus the NT group (6.67±0.53 % vs. 9.16±0.98 %, p protein expression of total eNOS and S1177 phosphorylated eNOS were not significantly different between the HTN and NT groups (0.46±0.07 vs. 0.38±0.05 and ±0.05 vs. 0.36±0.08, p = NS, respectively). In conclusion, our study suggests that impairment in the endothelial vasodilator function is independent of eNOS or S1177 phosphorylation of eNOS protein expression in human hypertension. Further studies are needed to clarify the molecular basis of endothelial dysfunction in hypertensive patients.