Effects of diadenosine polyphosphates on glomerular volume

1 Diadenosine polyphosphates (P1,P3‐diadenosine triphosphate, Ap3A; P1,P4‐diadenosine tetraphosphate, Ap4A; and P1,P5‐diadenosine pentaphosphate, Ap5A) are vasoactive molecules. The experimental model of isolated rat renal glomeruli was used to investigate their effects on glomerular vasculature. We...

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Published in:British journal of pharmacology 2005-04, Vol.144 (8), p.1109-1117
Main Authors: Szczepańska‐Konkel, Miroslawa, Jankowski, Maciej, Stiepanow‐Trzeciak, Anna, Angielski, Stefan
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Diadenosine polyphosphates
Dinucleoside Phosphates - pharmacology
Dose-Response Relationship, Drug
GIS
Kidney Glomerulus - blood supply
Kidney Glomerulus - drug effects
Kidney Glomerulus - physiology
Male
Medical sciences
Pharmacology. Drug treatments
purinoceptors
Rats
Rats, Wistar
renal glomeruli
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Summary:1 Diadenosine polyphosphates (P1,P3‐diadenosine triphosphate, Ap3A; P1,P4‐diadenosine tetraphosphate, Ap4A; and P1,P5‐diadenosine pentaphosphate, Ap5A) 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 Ap4A and Ap5A induced concentration‐ and time‐dependent reduction of GIS whereas Ap3A had no effect. The effects of Ap4A and Ap5A (both at 1 μM) were prevented by a nonselective P2 receptor antagonist, that is, suramin (10 μM) and P2Y receptor antagonist – reactive blue 2 (50 μM). However, the antagonist of P1 receptor, that is, theophylline (1 μM) and A1 receptor 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX; 10 μM) did not affect the responses of glomeruli to Ap4A or Ap5A. 3 Ap3A, in contrast to Ap4A and Ap5A, 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 P2Y1 receptor – MRS 2179 (10 μM). However, theophylline and the specific antagonist of A2 receptor – 3,7‐dimethyl‐1‐propargylxanthine (DMPX; 10 μM) – did not affect Ap3A action. 4 We indicate that diadenosine polyphosphates changed the glomerular volume via activation of P2 receptors. We suggest that extracellular Ap4A and Ap5A via P2X and P2Y receptors may decrease and Ap3A via, at least in part, P2Y1 receptors may increase filtration surface, which in turn may modify glomerular filtration rate. British Journal of Pharmacology (2005) 144, 1109–1117. doi:10.1038/sj.bjp.0706149
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0706149