Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium

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Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium. / Knapp, J; Bokník, P; Linck, B; Läer, S; Müller, F U; Neumann, J; Vahlensieck, U; Schlüter, H; Zidek, W; Schmitz, W.

in: N-S ARCH PHARMACOL, Jahrgang 360, Nr. 3, 09.1999, S. 354-7.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Knapp, J, Bokník, P, Linck, B, Läer, S, Müller, FU, Neumann, J, Vahlensieck, U, Schlüter, H, Zidek, W & Schmitz, W 1999, 'Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium', N-S ARCH PHARMACOL, Jg. 360, Nr. 3, S. 354-7.

APA

Knapp, J., Bokník, P., Linck, B., Läer, S., Müller, F. U., Neumann, J., Vahlensieck, U., Schlüter, H., Zidek, W., & Schmitz, W. (1999). Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium. N-S ARCH PHARMACOL, 360(3), 354-7.

Vancouver

Bibtex

@article{1a4a8e16dfce49ddb5e8766b5a2a39e7,
title = "Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium",
abstract = "In human ventricular trabeculae carneae 100 microM AP4A (diadenosine tetraphosphate) increased force of contraction to 162.8+/-15.7% of predrug value (n=9). This positive inotropic effect was accompanied by a prolongation of time parameters: time to peak tension and time of relaxation were prolonged by 7.8+/-1.3% and 14.9+/-3.8%, respectively (P<0.05). In the same trabeculae, AP4A increased IP3 (inositol-1,4,5-trisphosphate) content from 9.0+/-1.3 pmol/mg to 22.9+/-5.4 pmol/mg protein (n=5-9). In conclusion, the positive inotropic effect of AP4A in the human myocardium is likely due to an increase of IP3 mediated probably via Gq-coupled P2Y-purinoceptors. Because of the prominent role of Gq in the development of cardiac disease, these findings may lay the ground to further investigate the possible role of AP4A and/or related ligands (e.g. AP2A and AP3A) in heart failure.",
keywords = "Cardiomyopathies, Dinucleoside Phosphates, Electric Stimulation, Heart Ventricles, Humans, In Vitro Techniques, Inositol 1,4,5-Trisphosphate, Male, Middle Aged, Myocardial Contraction, Time Factors, Journal Article, Research Support, Non-U.S. Gov't",
author = "J Knapp and P Bokn{\'i}k and B Linck and S L{\"a}er and M{\"u}ller, {F U} and J Neumann and U Vahlensieck and H Schl{\"u}ter and W Zidek and W Schmitz",
year = "1999",
month = sep,
language = "English",
volume = "360",
pages = "354--7",
journal = "N-S ARCH PHARMACOL",
issn = "0028-1298",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Inositol-1,4,5-trisphosphate increase by diadenosine tetraphosphate in preparations from failing human myocardium

AU - Knapp, J

AU - Bokník, P

AU - Linck, B

AU - Läer, S

AU - Müller, F U

AU - Neumann, J

AU - Vahlensieck, U

AU - Schlüter, H

AU - Zidek, W

AU - Schmitz, W

PY - 1999/9

Y1 - 1999/9

N2 - In human ventricular trabeculae carneae 100 microM AP4A (diadenosine tetraphosphate) increased force of contraction to 162.8+/-15.7% of predrug value (n=9). This positive inotropic effect was accompanied by a prolongation of time parameters: time to peak tension and time of relaxation were prolonged by 7.8+/-1.3% and 14.9+/-3.8%, respectively (P<0.05). In the same trabeculae, AP4A increased IP3 (inositol-1,4,5-trisphosphate) content from 9.0+/-1.3 pmol/mg to 22.9+/-5.4 pmol/mg protein (n=5-9). In conclusion, the positive inotropic effect of AP4A in the human myocardium is likely due to an increase of IP3 mediated probably via Gq-coupled P2Y-purinoceptors. Because of the prominent role of Gq in the development of cardiac disease, these findings may lay the ground to further investigate the possible role of AP4A and/or related ligands (e.g. AP2A and AP3A) in heart failure.

AB - In human ventricular trabeculae carneae 100 microM AP4A (diadenosine tetraphosphate) increased force of contraction to 162.8+/-15.7% of predrug value (n=9). This positive inotropic effect was accompanied by a prolongation of time parameters: time to peak tension and time of relaxation were prolonged by 7.8+/-1.3% and 14.9+/-3.8%, respectively (P<0.05). In the same trabeculae, AP4A increased IP3 (inositol-1,4,5-trisphosphate) content from 9.0+/-1.3 pmol/mg to 22.9+/-5.4 pmol/mg protein (n=5-9). In conclusion, the positive inotropic effect of AP4A in the human myocardium is likely due to an increase of IP3 mediated probably via Gq-coupled P2Y-purinoceptors. Because of the prominent role of Gq in the development of cardiac disease, these findings may lay the ground to further investigate the possible role of AP4A and/or related ligands (e.g. AP2A and AP3A) in heart failure.

KW - Cardiomyopathies

KW - Dinucleoside Phosphates

KW - Electric Stimulation

KW - Heart Ventricles

KW - Humans

KW - In Vitro Techniques

KW - Inositol 1,4,5-Trisphosphate

KW - Male

KW - Middle Aged

KW - Myocardial Contraction

KW - Time Factors

KW - Journal Article

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

M3 - SCORING: Journal article

C2 - 10543439

VL - 360

SP - 354

EP - 357

JO - N-S ARCH PHARMACOL

JF - N-S ARCH PHARMACOL

SN - 0028-1298

IS - 3

ER -