Epithelial sodium channel activity is not increased in hypertension in whites

Abnormal renal sodium transport causing excess reabsorption of sodium may be one mechanism that causes high blood pressure. For example, increased activity of epithelial sodium channels in the distal tubule is the cause of high blood pressure in Liddle's syndrome, a rare familial form of hypertension. We have shown that the increase in sodium channel activity can be detected in the nose using transepithelial potential difference measurements in 1 family with Liddle's syndrome. We therefore used nasal potential difference measurements to look for increased sodium channel activity in white patients with essential hypertension. Transnasal potential difference was measured in 42 white hypertensive (HT) subjects and 38 white normotensive (NT) subjects before and after topical application of 10(-4) mol/L of amiloride. There was no difference in maximum potential between HT and NT subjects (HT, -18.8 +/- 0.9 mV; NT, -18.2 +/- 1.0 mV) (values mean +/- SEM; lumen-negative with respect to the submucosa). However, the postamiloride potential was significantly higher (HT, -12.6 +/- 0.7 mV; NT, -10.5 +/- 0.7 mV; P = 0.015) and the change in potential in response to amiloride significantly lower (HT, 6.2 +/- 0.5 mV, 33.1 +/- 2.08; NT, 7.7 +/- 0.6 mV, 41.9 +/- 2.0%; P = 0.046 and 0.003, respectively) in HT than in NT subjects. These results suggest that sodium channel activity is not increased in whites with essential hypertension and indicate that sodium channel overactivity similar to that seen in Liddle's syndrome is unlikely to be the cause of high blood pressure in this group. Increased postamiloride potential may reflect increased activity of chloride channels or amiloride-insensitive sodium channels.