Journal Article

Vasoactivity of diadenosine polyphosphates in human small renal resistance arteries

Martin Steinmetz, Gert Gabriëls, Truc Van Le, Hans-Jürgen Piechota, Karl Heinz Rahn and Eberhard Schlatter

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 18, issue 12, pages 2496-2504
Published in print December 2003 | ISSN: 0931-0509
Published online December 2003 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/gfg405
Vasoactivity of diadenosine polyphosphates in human small renal resistance arteries

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Background. We examined for the first time the vascular effects of purinergic agents that contribute to the regulation of peripheral vascular resistance in human small renal resistance arteries (hRRAs).

Methods and Results. Diadenosine polyphosphates (ApnAs, n = 3–6) and ATP, mounted in a microvessel myograph, caused vasoconstriction in hRRAs (rank order of potency: Ap5A > Ap6A= Ap4A > Ap3A= ATP). ADP, AMP and adenosine had less contractile potency than ApnA, suggesting that the observed effects were not induced by ApnA degradation products. The ApnA agent, Ap5A, but not Ap4A, induced vasoconstrictions that were inhibited by pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS; a P2X purinoceptor antagonist), but not by ADP3′5′ (a P2Y purinoceptor antagonist). In pre-contracted hRRAs, all of the ApnA agents caused vasorelaxation, and the potencies did not differ from each other. The ApnA degradation products had less vasorelaxing potencies than ApnA, suggesting that the vasorelaxation was caused by the ApnA agents themselves. Ap4A-induced vasorelaxation was inhibited by ADP3′5′ and PPADS. In contrast, Ap5A-induced vasorelaxation was not antagonized by ADP3′5′, but was antagonized more strongly by PPADS than was Ap4A.

Conclusions. We found that the tone of resistance arteries in human kidneys can be considerably influenced by these purinergic agonists, and most potently by ApnAs. Ap5A-induced vasoconstriction appeared to be mediated by P2X purinoceptors, whereas constriction due to Ap4A was caused by a different purinoceptor. Vasorelaxation due to Ap4A, but not Ap5A, appeared to be mediated by P2Y purinoceptors.

Keywords: ApnA; diadenosine polyphosphate; human kidney; human renal resistance artery; purinoceptor

Journal Article.  4725 words.  Illustrated.

Subjects: Nephrology

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