Effects of dinucleoside polyphosphates on regulation of coronary vascular tone
Standard
Effects of dinucleoside polyphosphates on regulation of coronary vascular tone. / van der Giet, Markus; Schmidt, Sven; Tölle, Markus; Jankowski, Joachim; Schlüter, Hartmut; Zidek, Walter; Tepel, Martin.
in: EUR J PHARMACOL, Jahrgang 448, Nr. 2-3, 19.07.2002, S. 207-13.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Effects of dinucleoside polyphosphates on regulation of coronary vascular tone
AU - van der Giet, Markus
AU - Schmidt, Sven
AU - Tölle, Markus
AU - Jankowski, Joachim
AU - Schlüter, Hartmut
AU - Zidek, Walter
AU - Tepel, Martin
N1 - Copyright 2002 Elsevier Science B.V.
PY - 2002/7/19
Y1 - 2002/7/19
N2 - The aim of the present study was to investigate the effects of Xp(5)X and Xp(6)X (X = guanosine (G) or adenosine (A); n = 5 and 6), which have been identified in human platelets, on coronary vascular tone. The activation of purinoceptors in rat coronary vasculature by Xp(5)X and Xp(6)X was evaluated by measuring their effects on perfusion pressure in the Langendorff perfused rat. Ap(5)X and Ap(6)X induced dose-dependent vasodilation that was due to P2Y(1) receptor activation, as evidenced by use of the selective P2Y(1) receptor antagonist 2'-deoxy-N(6)-methyl-adenosine 3',5'-diphosphate diammonium (MRS2179). Vasodilation was induced by NO release, as evidenced by inhibition of nitric oxide synthases (NO synthases) by N(G)-nitro-L-arginine methyl ester (L-NAME). The dose-dependent decrease in coronary perfusion pressure induced by Ap(5)X and Ap(6)X was converted to a dose-dependent increase in perfusion pressure after inhibition of NO synthases by L-NAME. After endothelium removal, the vasodilation elicited by Ap(5)X and Ap(6)X was converted to a vasoconstriction which could be inhibited by P2X receptor blockade. Ap(5)A, Ap(5)G, Ap(6)A and Ap(6)G are vasodilating or vasoconstricting nucleotides that activate P2Y(1) or P2X receptors depending on the status of the coronary vascular endothelium.
AB - The aim of the present study was to investigate the effects of Xp(5)X and Xp(6)X (X = guanosine (G) or adenosine (A); n = 5 and 6), which have been identified in human platelets, on coronary vascular tone. The activation of purinoceptors in rat coronary vasculature by Xp(5)X and Xp(6)X was evaluated by measuring their effects on perfusion pressure in the Langendorff perfused rat. Ap(5)X and Ap(6)X induced dose-dependent vasodilation that was due to P2Y(1) receptor activation, as evidenced by use of the selective P2Y(1) receptor antagonist 2'-deoxy-N(6)-methyl-adenosine 3',5'-diphosphate diammonium (MRS2179). Vasodilation was induced by NO release, as evidenced by inhibition of nitric oxide synthases (NO synthases) by N(G)-nitro-L-arginine methyl ester (L-NAME). The dose-dependent decrease in coronary perfusion pressure induced by Ap(5)X and Ap(6)X was converted to a dose-dependent increase in perfusion pressure after inhibition of NO synthases by L-NAME. After endothelium removal, the vasodilation elicited by Ap(5)X and Ap(6)X was converted to a vasoconstriction which could be inhibited by P2X receptor blockade. Ap(5)A, Ap(5)G, Ap(6)A and Ap(6)G are vasodilating or vasoconstricting nucleotides that activate P2Y(1) or P2X receptors depending on the status of the coronary vascular endothelium.
KW - Animals
KW - Coronary Vessels
KW - Dinucleoside Phosphates
KW - Dose-Response Relationship, Drug
KW - Endothelium, Vascular
KW - In Vitro Techniques
KW - Male
KW - Purinergic Agonists
KW - Rats
KW - Rats, Wistar
KW - Receptors, Purinergic
KW - Vasoconstriction
KW - Vasodilation
KW - Journal Article
M3 - SCORING: Journal article
C2 - 12144943
VL - 448
SP - 207
EP - 213
JO - EUR J PHARMACOL
JF - EUR J PHARMACOL
SN - 0014-2999
IS - 2-3
ER -
