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 < 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.
- © 2013 by American Heart Association, Inc.