Interaction of adenosine with vasopressin in the inner medullary collecting duct

Yoram Yagil

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Administra-tion of adenosine (Ado) into rat renal artery induces dosedependent diuresis that is independent of changes in glomerular filtration rate or renal blood flow, suggesting a direct effect on tubule H2O reabsorption. To test the hypothesis that Ado modulates cellular action of arginine vasopressin (AVP) as a tubular mechanism for the diuretic effect of Ado, interaction of Ado with AVP was studied in primary cell culture of rat inner medullary collecting duct (IMCD) epithelium. Stimulation of cells with 10-6 M AVP in presence of 0.1 mM Ro 20-1724, a nonmethylxanthine phosphodiesterase inhibitor that has no effect on Ado receptors, increased adenosine 3′,5′-cyclic monophosphate (cAMP) levels twofold or more above baseline. Stimulation of cells with the A1 Ado-receptor agonist N6cyclohexyladenosine (CHA), the A2-receptor agonist 5′-(N-ethylcarboxamido)-adenosine (NECA), or with the P-site agonist 2′,5′-dideoxyadenosine (DBA) significantly inhibited the AVP-stimulated cAMP response. Preincubation with pertussis toxin abolished the inhibitory effects of CHA and NECA, but not of DBA. The data suggest that, in the rat IMCB, Ado modulates AVP action by interfering with its ability to stimulate formation of its second messenger, cAMP. This effect is mediated by the extracellular Ado receptors A1 and A2 and by the intracellular P-site. It occurs by at least two pathways, one sensitive and the other insensitive to pertussis toxin.

Original languageEnglish
Pages (from-to)F679-F687
JournalAmerican Journal of Physiology - Renal Physiology
Volume259
Issue number4 28-4
StatePublished - 1 Jan 1990
Externally publishedYes

Keywords

  • 2′
  • 5′ (
  • 5′-cyclic monophosphate
  • 5′-dideoxyadenosine
  • Adenosine 3′
  • Arginine vasopressin
  • Cell culture
  • N-cyclohexyladenosine
  • N-ethylcarboxamido) -adenosine

ASJC Scopus subject areas

  • Physiology

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