Mechanism of Vasopressin-Induced Contraction of Renal Medullary Interstitial Cells

Abstract

Background/Aims: Previous studies have identified a contractile function for renomedullary interstitial cells (RMIC). Such studies focused on the mechanism of endothelin-1-induced RMIC contraction; however, vasopressin (AVP) was also noted to contract RMIC. Since AVP-induced RMIC contraction may be relevant to the medullary effects of AVP on urinary concentration, these initial observations have been extended to examination of the mechanism of AVP-induced RMIC contraction. Methods: Cultured rat RMIC were exposed to AVP and other agents, and examined using video microscopy. Results: AVP caused a slowly developing and dose-dependent reduction in RMIC surface area. AVP-induced RMIC contraction was abolished by blockade of V₁, but not V₂, receptors. Nifedipine and nickel reduced AVP-stimulated RMIC contraction, indicating that this effect is dependent upon dihydropyridine-sensitive calcium channels. H7, a protein kinase C inhibitor, completely abrogated AVP action, while the nitric oxide synthase inhibitor, NMMA, had no effect. Indomethacin enhanced AVP-induced RMIC contraction, and addition of PGE₂ together with indomethacin reduced AVP action. Conclusion: These data indicate that AVP potently contracts RMIC via V₁ receptor stimulation of PKC and intracellular calcium accumulation, and that AVP-stimulated prostaglandin production downregulates the contractile effect of AVP on RMIC. AVP modulation of RMIC contraction may be involved in the regulation of urinary concentration.

Journal

Journal ID (publisher-id): NEP

Journal ID (nlm-ta): Nephron Physiol

Journal ID (doi): 10.1159/issn.1660-2137

Title: Nephron Physiology

Publisher: S. Karger AG

ISSN (Electronic): 1660-2137

Publication date Subscription-year: 2006

Publication date (Print): June 2006

Publication date (Electronic): 22 June 2006

Volume: 103

Issue: 3

Pages: p119-p124

Affiliations

^aDepartment of Veterans Affairs Medical Center, ^bDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah, USA

Article

Publisher ID: 92245 Other ID: Nephron Physiol 2006;103:p119–p124

DOI: 10.1159/000092245

PubMed ID: 16557030

Copyright statement: © 2006 S. Karger AG, Basel

License:

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Page count

Figures: 5, References: 24, Pages: 1

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Categories

Subject: Original Paper