Role of nitric oxide in essential hypertension and its relationship to ventricular hypertrophy

Patients with essential hypertension exhibit blunted endothelium dependent vasodilator response, which is largely attributable to reduced bioavailability of nitric oxide [NO]. Therefore, this study was designed to estimate, more directly, nitric oxide production in patients with essential hypertension and to examine the possible association between NO and left ventrivular [LV] and vascular hypertrophy. The level of serum total nitrite and nitrate, the stable end products of NO oxidation, was measured in 40 hypertensive patients [group I] and 15 control subjects [group II]. Hypertensive patients were divided according to LV geometry into 21 patients with left ventricular hypertrophy [LVH] [group Ia] and 19 patients with normal LV geometry [group Ib]. Serum total nitrite and nitrate level was significantly lower in patients with essential hypertension compared to normal controls [25.07 +/- 8.78 micro mol/L verses 39.36 +/- 7.07 micro mol/L] [p<0.001]. It was significantly lower in patients with LVH compared to patients without LVH [20.50 +/- 8.07 micro mol/L versus 30.11 +/- 6.60 micro mol/L] [p<0.001]. There was a significant negative correlation between serum total nitrite and nitrate level and LVMI, IVS and PWT [p<0.001]. This study also showed a significant positive correlation between LVMI and carotid, femoral and aortic media to lumen [M/L] ratio [p<0.001]. Serum total nitrite and nitrate level was significantly lower in patients with higher M/L ratio and there was a significant negative correlation between serum total nitrite and nitrate level and carotid, femoral and aortic M/L ratio [p<0.01, p<0.001 and p<0.05 respectively]. It was concluded that NO level is reduced in patients with essential hypertension and that this reduced level has a role in the pathogenesis of left ventricular and vascular hy[ertrophy in patients with essential hyptertension