Effect of adenosine A1 analogue on tubuloglomerular feedback mechanism.

Academic Article

Abstract

  • To evaluate further the role of adenosine in the transmission of tubuloglomerular feedback signals, we studied the effects of an adenosine receptor antagonist and an adenosine A1-receptor agonist on feedback-mediated changes in stop-flow pressure (SFP). In orthograde perfusion experiments conducted in anesthetized rats, systemic administration of the adenosine receptor blocker 1,3-dipropyl-8-sulfophenylxanthine (PSPX) did not inhibit feedback responses. Control SFP feedback responses averaged 9.7 +/- 0.65 before and 8.6 +/- 0.55 mmHg during systemic infusion of the receptor blocker. In retrograde perfusion experiments, intratubular administration of the A1 agonist (360 nM) N6-cyclopentyladenosine (CPA), added to a hypotonic solution, markedly enhanced feedback responses. This effect was completely prevented by coinfusion of PSPX. Addition of 10 mM of the antagonist to the CPA-containing solution attenuated SFP feedback responses to less than 1 mmHg (delta = 0.44 +/- 0.50). Furthermore, PSPX also inhibited feedback responses obtained with an isotonic solution alone. Furosemide, which has been shown to block normal SFP responses obtained with isotonic solutions, failed to block CPA-induced decreases in SFP. These data demonstrate that intraluminal administration of an adenosine A1 analogue causes feedback-mediated decreases in SFP and therefore support a role for adenosine receptors in the signal transmission pathway.
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    Published In

    Keywords

  • Adenosine, Animals, Feedback, Hypertonic Solutions, Hypotonic Solutions, Kidney Glomerulus, Kidney Tubules, Male, Perfusion, Rats, Rats, Inbred Strains, Receptors, Purinergic, Xanthines
  • Digital Object Identifier (doi)

    Authorlist

  • Franco M; Bell PD; Navar LG
  • Start Page

  • F231
  • End Page

  • F236
  • Volume

  • 257
  • Issue

  • 2 Pt 2