HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ishikawa, S.-e Articles by Saito, T. Search for Related Content PubMed Articles by Ishikawa, S.-e Articles by Saito, T.

Biphasic effect of interleukin-1β on arginine vasopressin-induced cellular cyclic adenosine monophosphate production in cultured rat renal papillary collecting tubule cells

Ishikawa S, Saito T. Biphasic effect of interleukin-1β on arginine vasopressin-induced cellular cyclic adenosine monophosphate production in cultured rat renal papillary collecting tubule cells. Eur J Endocrinol 1995;132:472–8. ISSN 0804–4643

The present study was undertaken to determine whether interleukin (IL)-1β affects the response of cellular cyclic adenosine monophosphate production to arginine vasopressin (AVP) in cultured rat renal papillary collecting tubule cells. Arginine vasopressin increased cellular cAMP production in a dose-dependent manner. A 10-min exposure of cells to IL-1β at a concentration of 1 x 10^–12 mol/l or higher significantly reduced the AVP-induced increases in cellular cAMP production but did not affect the 2 x 10^–8 mol/l forskolin-induced increases in cellular cAMP production. The IL-1β inhibition disappeared totally when cells were pretreated with 100 µg/1 pertussis toxin for 2 h. In contrast, more than a 30-min exposure of cells to IL-1β increased basal cAMP levels and enhanced both the AVP- and forskolin-induced increases in cellular cAMP production. These results indicate that IL-1β produces biphasic regulation of AVP-induced cellular cAMP production in renal papillary collecting tubule cells. The inhibition by IL-1β is dependent on the activation of pertussis toxin-sensitive G protein. However, the mechanism whereby the longer exposure to IL-1β enhances cAMP production remains to be determined.

San-e Ishikawa, Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, 3311-1 Yakushiji Minamikawachi-machi, Tochigi 329-04. Japan