The epithelial sodium channel in hypertension.

Abstract:

:Our understanding of Na(+) transport defects has exploded in the past several years, and has provided unique insights into epithelial transport processes, and unusual clinical syndromes resulting from mutations of specific ion transporters. These genetic disorders affect Na(+) balance, with both Na(+) retaining and Na(+) wasting conditions being the consequence. A major focus of these studies has been the epithelial sodium channel (ENaC), which can be directly affected by mutations (eg, Liddle syndrome, autosomal recessive pseudohypoaldosteronism, type I) or by changes in the response to (autosomal recessive pseudohypoaldosteronism, type I), or production of mineralocorticoids (apparent mineralocorticoid excess syndrome, glucocorticoid-remediable aldosteronism). As a result, we now have clearly defined syndromes in which ENaC activity is dysregulated with subsequent development of disorders of systemic blood pressure that can be attributed to a primary renal mechanism.

journal_name

Curr Hypertens Rep

authors

Warnock DG

doi

10.1007/s11906-999-0013-x

keywords:

subject

Has Abstract

pub_date

1999-04-01 00:00:00

pages

158-63

issue

2

eissn

1522-6417

issn

1534-3111

journal_volume

1

pub_type

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