Racial difference in the activity of the amiloride-sensitive epithelial sodium channel.

نویسندگان

  • J Howard Pratt
  • Walter T Ambrosius
  • Rajiv Agarwal
  • George J Eckert
  • Shirley Newman
چکیده

Compared with whites, blacks appear to retain additional sodium that suppresses secretion of renin and aldosterone. The epithelial sodium channel (ENaC) is an aldosterone-regulated site for sodium reabsorption. ENaC activity could be higher in blacks, contributing to sodium retention or, alternatively, lower because of reduced stimulation by aldosterone. To examine the level of ENaC activity in blacks relative to whites, blood pressure (BP) responses to amiloride (5 mg/d), an inhibitor of ENaC, were measured in 20 black and 25 white normotensive young people. After 1 week, systolic BP decreased by 3.0+/-9.2 (SD) and diastolic by 2.8+/-8.3 mm Hg in the whites, whereas systolic BP increased by 2.5+/-7.1 and diastolic by 3.8+/-8.0 mm Hg in the blacks; the racial difference in the BP response was significant for both systolic (P=0.034) and diastolic BP (P=0.010). As ENaC activity increases, renal secretion of potassium increases proportionately, and in a larger sample of subjects, the urinary potassium excretion rate was lower in the blacks (n=301) than in the whites (n=461): 3.2+/-0.1 versus 3.8+/-0.1 mmol/mmol creatinine (P=0.0001). The concentration of serum potassium was higher in the blacks (n=81) than in the whites (n=167): 4.36+/-0.05 versus 4.21+/-0.03 (P=0.012). In summary, a favorable BP response to amiloride in the whites as well as the evidence for greater retention of potassium in the blacks is consistent with blacks having less ENaC activity than whites. We suggest that increased sodium retention in blacks occurring at other nephron sites suppresses aldosterone secretion and in turn ENaC function.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Modulation of epithelial Na+ channel activity by long-chain n-3 fatty acids.

The epithelial sodium channel is found in apical membranes of a variety of native epithelial tissues, where it regulates sodium and fluid balance. In vivo, a number of hormones and other endogenous factors, including polyunsaturated fatty acids (PUFAs), regulate these channels. We tested the effects of essential n-3 and n-6 PUFAs on amiloride-sensitive sodium transport in A6 epithelial cells. E...

متن کامل

Primary structure of an apical protein from Xenopus laevis that participates in amiloride-sensitive sodium channel activity

High resistance epithelia express on their apical side an amiloride-sensitive sodium channel that controls sodium reabsorption. A cDNA was found to encode a 1,420-amino acid long polypeptide with no signal sequence, a putative transmembrane segment, and three predicted amphipathic alpha helices. A corresponding 5.2-kb mRNA was detected in Xenopus laevis kidney, intestine, and oocytes, with weak...

متن کامل

The amiloride-sensitive epithelial Na+ channel PPK28 is essential for drosophila gustatory water reception.

Water sensation is a specific taste modality in the fruit fly. Water-induced hypoosmolarity activates specific gustatory receptor neurons; however, the molecular identity of the putative osmolarity sensor in these neurons remains unknown. We found that amiloride and its analogs specifically antagonized the response of water gustatory receptor neurons and the behavior of flies toward water stimu...

متن کامل

Downregulation of ENaC activity and expression by TNF- in alveolar epithelial cells

Dagenais, André, Rosalie Fréchette, Yuko Yamagata, Toshiyuki Yamagata, Jean-François Carmel, Marie-Eve Clermont, Emmanuelle Brochiero, Chantal Massé, and Yves Berthiaume. Downregulation of ENaC activity and expression by TNFin alveolar epithelial cells. Am J Physiol Lung Cell Mol Physiol 286: L301–L311, 2004. First published September 26, 2003; 10.1152/ ajplung.00326.2002.—Sodium absorption by ...

متن کامل

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 t...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Hypertension

دوره 40 6  شماره 

صفحات  -

تاریخ انتشار 2002