This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Baxendale-Cox, L. M. Articles by Duncan, R. L. Search for Related Content PubMed PubMed Citation Articles by Baxendale-Cox, L. M. Articles by Duncan, R. L. Social Bookmarking                         What's this?

Insulin Increases Sodium (Na+) Channel Density in A6 Epithelia: Implications for Expression of Hypertension

HPE and related brain malformations, Kennedy Krieger Institute, Baltimore, MD.

Randall L. Duncan, PhD

Department of Orthopedic Surgery, Indiana University School of Medicine.

Essential or primary hypertension is a multifactorial disease that is expressed as a result of complex interactions between genes and environmental influences. Several mutations in many different proteins are associated with expression of hypertension, including abnormalities in the epithelial sodium channel (ENaC) found in absorptive organs (i.e., distal colon, distal tubule of the nephron). Some of these mutations result in structural and/or functional alterations in ENaC-mediated Na+ entry in epithelia responsible for fluid and electrolyte balance and are associated with expression of hypertension. Studies support the notion that there is a link between ENaC and hypertension of both the monogenic (single gene mutation) and primary or essential type (a multifactorial disease). Alterations of other aspects of the environment of absorptive cells (e.g., hyperinsulinemia, hyperaldosteronemia, high plasma cortisol, high plasma Na+) have also been shown to elicit hyperabsorption of Na+ via ENaC and therefore could contribute significantly to expression of hypertension in people with intermediate phenotypes. This article describes an initial study in which the effects of an environmental factor, extracellular levels of insulin, on ENaC were examined in a normal kidney cell model. Electrophysiologic techniques revealed that ENaC density rapidly increased in response to addition of insulin to the basolateral bath. This autoregulatory recruitment of Na+ total channel density masked a slight decrease in open channel probability. Insulin’s effect on ENaC function and implications on fluid and electrolyte balance and expression of primary hypertension is discussed.

Key Words: Sodium transport • renal epithelium • sodium channel • cultured epithelial cells • hypertension • insulin

Biological Research For Nursing, Vol. 1, No. 1, 20-29 (1999)
DOI: 10.1177/109980049900100104


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				N. Y. Tallini and L. C. Stoner Amiloride-sensitive sodium current in everted Ambystoma initial collecting tubule: short-term insulin effects Am J Physiol Cell Physiol, October 1, 2002; 283(4): C1171 - C1181. [Abstract] [Full Text] [PDF]