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Vol. 294, Issue 3, 1182-1187, September 2000
Medizinische Poliklinik, Westfälische
Wilhelms-Universität Münster, Münster, Germany
In the accompanying article, we showed that AP5A displayed heterogenous
vasoactive effects in rat resistance arteries. It induced a stable
vasoconstriction in the superior epigastric artery (SEA) and a
transient vasoconstriction in the mesenteric resistance artery (MrA).
In the phenylephrine-precontracted MrA AP5A induced a marked
vasorelaxation. In this study the noncompetitive inhibition of the
AP5A-induced vasoconstriction with
pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid was found
to be significantly stronger in MrA than in SEA. The nonselective P2
purinoceptor antagonist suramin inhibited AP5A-induced vasoconstriction
in MrA only. The vasoconstriction by the P2X purinoceptor agonist
,
-methylene ATP was inhibited by with
pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and suramin
similarly to that induced by AP5A. Thus, the AP5A-induced vasoconstriction is due to P2X receptor activation, but two different P2X receptors seem to be operational in the two different vessels. The
AP5A-induced vasorelaxation of phenylephrine-precontracted MrA was
inhibited by the P2Y1 receptor antagonist ADP3'5'. The vasorelaxation induced by ADPS (P2Y1 agonist) also was
inhibited by ADP3'5'. These findings suggest that AP5A-induced
vasorelaxation of MrA is caused by P2Y1 receptor
activation. The P1 (A2) receptor antagonist
3,7-dimethyl-1-propargylxanthine only slightly inhibited AP5A-induced
vasorelaxation at high concentrations. Adenosine and the A2
receptor agonist CGS21680 failed to produce significant vasorelaxation.
Therefore, vasorelaxation in MrA does not involve A2
purinoceptor activation. AP5A-induced vasorelaxation was not inhibited
by Ca2+- or ATP-dependent K+ channel blockade
with clotrimazole, apamin, or glibenclamide. These data indicate that
vasoconstriction in MrA and SEA by AP5A is due to different P2X
receptors, and vasorelaxation in precontracted MrA is due to
P2Y1 receptor activation.
This article has been cited by other articles:
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  M. Steinmetz, G. Gabriels, T. V. Le, H.-J. Piechota, K. H. Rahn, and E. Schlatter Vasoactivity of diadenosine polyphosphates in human small renal resistance arteries Nephrol. Dial. Transplant., December 1, 2003; 18(12): 2496 - 2504. [Abstract] [Full Text] [PDF]
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 G. Gabriels, K. H. Rahn, E. Schlatter, and M. Steinmetz Mesenteric and renal vascular effects of diadenosine polyphosphates (APnA) Cardiovasc Res, October 1, 2002; 56(1): 22 - 32. [Abstract] [Full Text] [PDF]
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M. Steinmetz, T. Van Le, P. Hollah, G. Gabriëls, H. Hohage, K. H. Rahn, and E. Schlatter Influence of Purinoceptor Antagonism on Diadenosine Pentaphosphate-Induced Hypotension in Anesthetized Rats J. Pharmacol. Exp. Ther., September 1, 2000; 294(3): 963 - 968. [Abstract] [Full Text]
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M. Steinmetz, E. Schlatter, H. A. J. S. Boudier, K. H. Rahn, and J. G. R. De Mey Diadenosine Polyphosphates Cause Contraction and Relaxation in Isolated Rat Resistance Arteries J. Pharmacol. Exp. Ther., September 1, 2000; 294(3): 1175 - 1181. [Abstract] [Full Text]
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