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

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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 < 0.05). Despite impairment in endothelial function, we found that

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.

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