Adenosine receptor-mediated inhibition of inositol 1,4,5 trisphosphate production in coronary artery

S. J. Mustafa, W. Abebe

Research output: Contribution to journalArticle

Abstract

Previously, we indirectly showed that relaxation of porcine coronary artery by adenosine and its analogs are linked to modulation of phospholipase C and protein kinase C. In the present investigation, we assessed if the relaxant responses to the adenosine analogs CAD and NECA are associated with inhibition of inositol 1,4,5-trisphosphate (IP3) formation. A protein binding assay system was used to measure the concentration of IP3. IP, was generated by prostaglandin F (20 μM) in coronary rings with and without endothelium. In both tissues, PGF caused a rapid and transient elevation of IP3 which reached a peak at 10 sec. Preincubation of tissues with either CAD or NECA caused a dose-related inhibition of the IP3 produced by PGF with a significant inhibition at higher doses. However, the inhibitory effect of NECA was relatively less in endothelium-intact rings. In addition, NECA by itself tended to increase the levels of basal IP3 in the intact but not denuded tissues. CAD did not produce a significant effect on the basal IP3 contents in both preparations. These results suggest that adenosine receptor activation in porcine coronary artery inhibits agonist-induced production of IP3, and the magnitude of inhibition appears to depend on the type of adenosine analog used and on the presence and absence of endothelium. (Supported by HL-27339 and Minority Supplement to HI.-50049).

Original languageEnglish (US)
Pages (from-to)A49
JournalFASEB Journal
Volume10
Issue number3
Publication statusPublished - Dec 1 1996
Externally publishedYes

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ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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