ArticleBritish journal of pharmacology2005
Effects of diadenosine polyphosphates on glomerular volume.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Redox regulation of hemodynamics response to diadenosine tetraphosphate an agonist of P2 receptors and renal function in diet-induced hypercholesterolemic rats.Physiological reports · 2021Article
- Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Physiological roles and potential therapeutic applications of the P2X7 receptor in inflammation and pain.Molecules (Basel, Switzerland) · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Diadenosine polyphosphates (P(1),P(3)-diadenosine triphosphate, Ap(3)A; P(1),P(4)-diadenosine tetraphosphate, Ap(4)A; and P(1),P(5)-diadenosine pentaphosphate, Ap(5)A) are vasoactive molecules. The experimental model of isolated rat renal glomeruli was used to investigate their effects on glomerular vasculature. We measured the changes of glomerular inulin space (GIS) as a marker of glomeruli contractility. 2. Ap(4)A and Ap(5)A induced concentration- and time-dependent reduction of GIS whereas Ap(3)A had no effect. The effects of Ap(4)A and Ap(5)A (both at 1 microM) were prevented by a nonselective P2 receptor antagonist, that is, suramin (10 microM) and P2Y receptor antagonist - reactive blue 2 (50 microM). However, the antagonist of P1 receptor, that is, theophylline (1 microM) and A(1) receptor 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 10 microM) did not affect the responses of glomeruli to Ap(4)A or Ap(5)A. 3. Ap(3)A, in contrast to Ap(4)A and Ap(5)A, prevented angiotensin II-induced reduction of GIS in a concentration- and time-dependent manner. This effect was partially prevented by suramin and markedly reduced by reactive blue 2 and the specific antagonist of P2Y(1) receptor - MRS 2179 (10 microM). However, theophylline and the specific antagonist of A(2) receptor - 3,7-dimethyl-1-propargylxanthine (DMPX; 10 microM) - did not affect Ap(3)A action. 4. We indicate that diadenosine polyphosphates changed the glomerular volume via activation of P2 receptors. We suggest that extracellular Ap(4)A and Ap(5)A via P2X and P2Y receptors may decrease and Ap(3)A via, at least in part, P2Y(1) receptors may increase filtration surface, which in turn may modify glomerular filtration rate.
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