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The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney

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The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney. / van der Giet, M; Westhoff, T; Cinkilic, O; Jankowski, J; Schlüter, H; Zidek, W; Tepel, M.

in: BRIT J PHARMACOL, Jahrgang 132, Nr. 2, 01.2001, S. 467-74.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

van der Giet, M, Westhoff, T, Cinkilic, O, Jankowski, J, Schlüter, H, Zidek, W & Tepel, M 2001, 'The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney', BRIT J PHARMACOL, Jg. 132, Nr. 2, S. 467-74. https://doi.org/10.1038/sj.bjp.0703817

APA

van der Giet, M., Westhoff, T., Cinkilic, O., Jankowski, J., Schlüter, H., Zidek, W., & Tepel, M. (2001). The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney. BRIT J PHARMACOL, 132(2), 467-74. https://doi.org/10.1038/sj.bjp.0703817

Vancouver

van der Giet M, Westhoff T, Cinkilic O, Jankowski J, Schlüter H, Zidek W et al. The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney. BRIT J PHARMACOL. 2001 Jan;132(2):467-74. https://doi.org/10.1038/sj.bjp.0703817

Bibtex

@article{926c9e39062649e0b0cce0ca7a7af0fe,
title = "The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney",
abstract = "1. The activation of P(2x)-receptors in the rat renal vasculature by dinucleoside polyphosphates with variable phosphate group chain length (Xp(n)X; X=Adenin (A) /Guanin (G), n=4 - 6) was studied by measuring their effects on perfusion pressure of the isolated perfused rat kidney at constant flow in an open circuit. 2. Like Ap(4)A, Ap(5)A and Ap(6)A the dinucleoside polyphosphates Ap(4)G, Ap(5)G and Ap(6)G exerted a vasoconstriction which could be blocked by suramin and pyridoxal-phosphate-6-azophenyl-2; 4-disulphonic acid (PPADS). 3. Gp(4)G, Gp(5)G and Gp(6)G showed only very weak vasoconstriction at high doses. 4. Ap(6)A and alpha, beta-meATP could not be blocked by the selective P(2x1)-receptor antagonisten NF023 (30 microM), whereas Ap(4)A, Ap(4)G, Ap(5)A, Ap(5)G and Ap(6)G were partially blocked by NF023. 5. Inhibition of endothelial NO-synthase by N(omega)-nitro-L-arginine methyl ester (L-NAME) did not affect vasoconstrictions induced by dinucleosidepolyphosphates. 6. P(2x)-receptor can only be activated if at least one adenosine moiety is present in the molecule. 7. Ap(n)G show a weaker vasoconstrictive action than corresponding Ap(n)A, concluding that two adenosine moieties enhance the P(2x)-receptor binding and activation. 8. Xp(n)X containing five phosphate groups show the most pronounced vasoconstrictive effect whereas four phosphate groups show the less effect, therefore the number of phosphate groups critically changes receptor affinity. 9. Additional experiments using permanent perfusion with alpha, beta-methylene ATP (alpha,beta-meATP) and the selective P(2x1)-receptor antagonist NF023 showed that the newly discovered human dinucleoside polyphosphates activated the vascular P(2x1)-receptor and an recently identified new P(2x)-receptor subtype. 10. The differential effects of dinucleoside polyphosphates allow a fine tuning of local perfusion via composition of Xp(n)Xs.",
keywords = "Adenosine, Adenosine Triphosphate, Animals, Dinucleoside Phosphates, Edema, Enzyme Inhibitors, Guanosine, In Vitro Techniques, Kidney, Male, Muscle Tonus, NG-Nitroarginine Methyl Ester, Nitric Oxide Synthase, Nitric Oxide Synthase Type III, Perfusion, Purinergic P1 Receptor Antagonists, Purinergic P2 Receptor Antagonists, Rats, Rats, Inbred WKY, Receptors, Purinergic P2, Vasoconstrictor Agents, Journal Article, Research Support, Non-U.S. Gov't",
author = "{van der Giet}, M and T Westhoff and O Cinkilic and J Jankowski and H Schl{\"u}ter and W Zidek and M Tepel",
year = "2001",
month = jan,
doi = "10.1038/sj.bjp.0703817",
language = "English",
volume = "132",
pages = "467--74",
journal = "BRIT J PHARMACOL",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - The critical role of adenosine and guanosine in the affinity of dinucleoside polyphosphates to P(2X)-receptors in the isolated perfused rat kidney

AU - van der Giet, M

AU - Westhoff, T

AU - Cinkilic, O

AU - Jankowski, J

AU - Schlüter, H

AU - Zidek, W

AU - Tepel, M

PY - 2001/1

Y1 - 2001/1

N2 - 1. The activation of P(2x)-receptors in the rat renal vasculature by dinucleoside polyphosphates with variable phosphate group chain length (Xp(n)X; X=Adenin (A) /Guanin (G), n=4 - 6) was studied by measuring their effects on perfusion pressure of the isolated perfused rat kidney at constant flow in an open circuit. 2. Like Ap(4)A, Ap(5)A and Ap(6)A the dinucleoside polyphosphates Ap(4)G, Ap(5)G and Ap(6)G exerted a vasoconstriction which could be blocked by suramin and pyridoxal-phosphate-6-azophenyl-2; 4-disulphonic acid (PPADS). 3. Gp(4)G, Gp(5)G and Gp(6)G showed only very weak vasoconstriction at high doses. 4. Ap(6)A and alpha, beta-meATP could not be blocked by the selective P(2x1)-receptor antagonisten NF023 (30 microM), whereas Ap(4)A, Ap(4)G, Ap(5)A, Ap(5)G and Ap(6)G were partially blocked by NF023. 5. Inhibition of endothelial NO-synthase by N(omega)-nitro-L-arginine methyl ester (L-NAME) did not affect vasoconstrictions induced by dinucleosidepolyphosphates. 6. P(2x)-receptor can only be activated if at least one adenosine moiety is present in the molecule. 7. Ap(n)G show a weaker vasoconstrictive action than corresponding Ap(n)A, concluding that two adenosine moieties enhance the P(2x)-receptor binding and activation. 8. Xp(n)X containing five phosphate groups show the most pronounced vasoconstrictive effect whereas four phosphate groups show the less effect, therefore the number of phosphate groups critically changes receptor affinity. 9. Additional experiments using permanent perfusion with alpha, beta-methylene ATP (alpha,beta-meATP) and the selective P(2x1)-receptor antagonist NF023 showed that the newly discovered human dinucleoside polyphosphates activated the vascular P(2x1)-receptor and an recently identified new P(2x)-receptor subtype. 10. The differential effects of dinucleoside polyphosphates allow a fine tuning of local perfusion via composition of Xp(n)Xs.

AB - 1. The activation of P(2x)-receptors in the rat renal vasculature by dinucleoside polyphosphates with variable phosphate group chain length (Xp(n)X; X=Adenin (A) /Guanin (G), n=4 - 6) was studied by measuring their effects on perfusion pressure of the isolated perfused rat kidney at constant flow in an open circuit. 2. Like Ap(4)A, Ap(5)A and Ap(6)A the dinucleoside polyphosphates Ap(4)G, Ap(5)G and Ap(6)G exerted a vasoconstriction which could be blocked by suramin and pyridoxal-phosphate-6-azophenyl-2; 4-disulphonic acid (PPADS). 3. Gp(4)G, Gp(5)G and Gp(6)G showed only very weak vasoconstriction at high doses. 4. Ap(6)A and alpha, beta-meATP could not be blocked by the selective P(2x1)-receptor antagonisten NF023 (30 microM), whereas Ap(4)A, Ap(4)G, Ap(5)A, Ap(5)G and Ap(6)G were partially blocked by NF023. 5. Inhibition of endothelial NO-synthase by N(omega)-nitro-L-arginine methyl ester (L-NAME) did not affect vasoconstrictions induced by dinucleosidepolyphosphates. 6. P(2x)-receptor can only be activated if at least one adenosine moiety is present in the molecule. 7. Ap(n)G show a weaker vasoconstrictive action than corresponding Ap(n)A, concluding that two adenosine moieties enhance the P(2x)-receptor binding and activation. 8. Xp(n)X containing five phosphate groups show the most pronounced vasoconstrictive effect whereas four phosphate groups show the less effect, therefore the number of phosphate groups critically changes receptor affinity. 9. Additional experiments using permanent perfusion with alpha, beta-methylene ATP (alpha,beta-meATP) and the selective P(2x1)-receptor antagonist NF023 showed that the newly discovered human dinucleoside polyphosphates activated the vascular P(2x1)-receptor and an recently identified new P(2x)-receptor subtype. 10. The differential effects of dinucleoside polyphosphates allow a fine tuning of local perfusion via composition of Xp(n)Xs.

KW - Adenosine

KW - Adenosine Triphosphate

KW - Animals

KW - Dinucleoside Phosphates

KW - Edema

KW - Enzyme Inhibitors

KW - Guanosine

KW - In Vitro Techniques

KW - Kidney

KW - Male

KW - Muscle Tonus

KW - NG-Nitroarginine Methyl Ester

KW - Nitric Oxide Synthase

KW - Nitric Oxide Synthase Type III

KW - Perfusion

KW - Purinergic P1 Receptor Antagonists

KW - Purinergic P2 Receptor Antagonists

KW - Rats

KW - Rats, Inbred WKY

KW - Receptors, Purinergic P2

KW - Vasoconstrictor Agents

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/sj.bjp.0703817

DO - 10.1038/sj.bjp.0703817

M3 - SCORING: Journal article

C2 - 11159696

VL - 132

SP - 467

EP - 474

JO - BRIT J PHARMACOL

JF - BRIT J PHARMACOL

SN - 0007-1188

IS - 2

ER -