This Article Full Text Full Text (PDF) 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 Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Husted, R. F. Articles by Stokes, J. B. Search for Related Content PubMed PubMed Citation Articles by Husted, R. F. Articles by Stokes, J. B. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Genes and Gene Therapy Hazardous Substances DB SODIUM SODIUM CHLORIDE

(Hypertension. 1998;31:608-614.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Candidate Genes in the Regulation of Na⁺ Transport by Inner Medullary Collecting Duct Cells From Dahl Rats

Russell F. Husted; John P. Rapp; ; John B. Stokes

From the Laboratory of Epithelial Transport, Department of Internal Medicine, University of Iowa, Iowa City (J.B.S., R.F.H.); the Department of Veterans Affairs Medical Center, Iowa City, IA (J.B.S.); and Department of Physiology, Medical College of Ohio, Toledo (J.P.R.).

Correspondence to John B. Stokes, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242.

Abstract—Recently, we reported that primary cultures of inner medullary collecting duct cells from Dahl salt-sensitive (S) rats absorb more Na⁺ than do cells cultured from Dahl salt-resistant (R) rats. To begin to evaluate the molecular basis for this difference, we selected four candidate gene products that on the basis of their physiology and genetics could participate in regulation of Na⁺ transport by these cells. During 24-hour exposure, inhibitors of the cytochrome P450 enzymes had no effect on Na⁺ transport by either S or R monolayers. Twenty-four-hour exposure to N^G-monomethyl-L-arginine (0.5 mmol/L), a nonspecific inhibitor of NO synthase, also had no effect on Na⁺ transport by either S or R monolayers. Neither atrial natriuretic peptide 1–28 (100 nmol/L) nor 8-Br-cyclic GMP (100 µmol/L) had any short-term effect on Na⁺ transport by either S or R monolayers. 18-Hydroxy-11-deoxycorticosterone (100 nmol/L), an adrenocorticoid hormone that is produced in greater amounts in S rats, stimulated Na⁺ transport by both S and R monolayers via the mineralocorticoid receptor; however, its effect was less potent than aldosterone. Congenic rats in which the R isoform of the 11ß-hydroxylase gene was bred onto the S background had monolayers that transported Na⁺ at a rate similar to the S rats. These results demonstrate that neither cytochrome P450 genes, NO synthase genes, the atrial natriuretic peptide receptor gene, nor the 11ß-hydroxylase gene is a likely candidate to explain the difference in Na⁺ transport between S and R inner medullary collecting duct monolayers in primary culture.

Key Words: atrial natriuretic peptides • nitric oxide synthase • cyclic GMP • 11ß-hydroxylase • rats, congenic • cell culture • electrophysiology

This article has been cited by other articles:

				R. F. Husted, C. Zhang, and J. B. Stokes Concerted actions of IL-1beta inhibit Na+ absorption and stimulate anion secretion by IMCD cells Am J Physiol Renal Physiol, December 1, 1998; 275(6): F946 - F954. [Abstract] [Full Text] [PDF]