Effects of adenosine on ion transport in rat medullary thick ascending limb

R. E. Beach, D. W. Good

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Previously, we demonstrated that adenosine (Ado) was released by the medullary thick ascending limb (MTAL) during hypoxia. The present experiments were designed to examine the effects of Ado and adenosine analogues on net chloride (J(Cl)) and bicarbonate (J(HCO3)) absorption by the isolated, perfused MTAL of the rat. Ado, 10 nM, in the presence or absence of arginine vasopressin (AVP, 10-10 M) reduced J(Cl) by 50%. The inhibition by Ado was reproduced with the selective A1 agonist, N-6-phenylisopropyladenine (2 nM), and was reversed by 8-cyclopentyl-1,3-dipropylxanthine, an A1-receptor antagonist. Thus the inhibition of J(Cl) is likely mediated through A1 receptors. In contrast, Ado had no effect on (J(HCO3)) either in the presence or absence of AVP. Ado also had no influence on the effect of AVP to inhibit J(HCO3). The lack of effect on J(HCO3) suggests that the inhibition of J(Cl) by Ado is unlikely to be mediated through changes in cellular adenosine 3',5'-cyclic monophosphate. These results support the hypothesis that Ado released into the renal medulla during hypoxia may protect the MTAL from ischemic injury by directly inhibiting NaCl absorption and reducing transport-related oxygen consumption.

Original languageEnglish (US)
Pages (from-to)F482-F487
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number3 32-3
StatePublished - 1992


  • adenosine 3',5'-cyclic monophosphate
  • bicarbonate transport
  • chloride transport
  • ischemic injury
  • loop of Henle
  • renal metabolism
  • transport-related oxygen consumption

ASJC Scopus subject areas

  • Physiology


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