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Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations

Standard

Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations. / Vahlensieck, U; Bokník, P; Gombosová, I; Huke, S; Knapp, J; Linck, B; Lüss, H; Müller, F U; Neumann, J; Deng, M C; Scheld, H H; Jankowski, H; Schlüter, H; Zidek, W; Zimmermann, N; Schmitz, W.

in: The Journal of pharmacology and experimental therapeutics, Jahrgang 288, Nr. 2, 02.1999, S. 805-13.

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

Harvard

Vahlensieck, U, Bokník, P, Gombosová, I, Huke, S, Knapp, J, Linck, B, Lüss, H, Müller, FU, Neumann, J, Deng, MC, Scheld, HH, Jankowski, H, Schlüter, H, Zidek, W, Zimmermann, N & Schmitz, W 1999, 'Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations', The Journal of pharmacology and experimental therapeutics, Jg. 288, Nr. 2, S. 805-13.

APA

Vahlensieck, U., Bokník, P., Gombosová, I., Huke, S., Knapp, J., Linck, B., Lüss, H., Müller, F. U., Neumann, J., Deng, M. C., Scheld, H. H., Jankowski, H., Schlüter, H., Zidek, W., Zimmermann, N., & Schmitz, W. (1999). Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations. The Journal of pharmacology and experimental therapeutics, 288(2), 805-13.

Vancouver

Vahlensieck U, Bokník P, Gombosová I, Huke S, Knapp J, Linck B et al. Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations. The Journal of pharmacology and experimental therapeutics. 1999 Feb;288(2):805-13.

Bibtex

@article{e0d970e936cf427e9d4cf3b55a81d3c9,
title = "Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations",
abstract = "Diadenosine tetraphosphate (AP4A) is an endogenous compound and exerts diverse physiological effects in animal systems. However, the effects of AP4A on inotropy in ventricular cardiac preparations have not yet been studied. The effects of AP4A on force of contraction (FOC) were studied in isolated electrically driven guinea pig and human cardiac preparations. Furthermore, the effects of AP4A on L-type calcium current and [Ca]i were studied in isolated guinea pig ventricular myocytes. In guinea pig left atria, AP4A (0.1-100 microM) reduced FOC maximally by 36.5 +/- 4.3%. In guinea pig papillary muscles, AP4A (100 microM) alone was ineffective, but reduced isoproterenol-stimulated FOC maximally by 29.3 +/- 3.4%. The negative inotropic effects of AP4A in atria and papillary muscles were abolished by the A1-adenosine receptor antagonist 1, 3-dipropyl-cyclopentylxanthine. In guinea pig ventricular myocytes, AP4A (100 microM) attenuated isoproterenol-stimulated L-type calcium current and [Ca]i. In human atrial and ventricular preparations, AP4A (100 microM) alone increased FOC to 158.3 +/- 12.4% and 167.5 +/- 25.1%, respectively. These positive inotropic effects were abolished by the P2-purinoceptor antagonist suramin. On the other hand, AP4A (100 microM) reduced FOC by 27.2 +/- 7.4% in isoproterenol-stimulated human ventricular trabeculae. The latter effect was abolished by 1,3-dipropyl-cyclopentylxanthine. In summary, after beta adrenergic stimulation AP4A exerts negative inotropic effects in animal and human ventricular preparations via stimulation of A1-adenosine receptors. In contrast, AP4A alone can exert positive inotropic effects via P2-purinoceptors in human ventricular myocardium. Thus, P2-purinoceptor stimulation might be a new positive inotropic principle in the human myocardium.",
keywords = "Animals, Calcium, Calcium Channels, Cells, Cultured, Dinucleoside Phosphates, Drug Interactions, Guinea Pigs, Heart, Heart Atria, Heart Ventricles, Humans, In Vitro Techniques, Male, Myocardial Contraction, Myocardium, Platelet Aggregation Inhibitors, Xanthines, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't",
author = "U Vahlensieck and P Bokn{\'i}k and I Gombosov{\'a} and S Huke and J Knapp and B Linck and H L{\"u}ss and M{\"u}ller, {F U} and J Neumann and Deng, {M C} and Scheld, {H H} and H Jankowski and H Schl{\"u}ter and W Zidek and N Zimmermann and W Schmitz",
year = "1999",
month = feb,
language = "English",
volume = "288",
pages = "805--13",
journal = "J PHARMACOL EXP THER",
issn = "0022-3565",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "2",

}

RIS

TY - JOUR

T1 - Inotropic effects of diadenosine tetraphosphate (AP4A) in human and animal cardiac preparations

AU - Vahlensieck, U

AU - Bokník, P

AU - Gombosová, I

AU - Huke, S

AU - Knapp, J

AU - Linck, B

AU - Lüss, H

AU - Müller, F U

AU - Neumann, J

AU - Deng, M C

AU - Scheld, H H

AU - Jankowski, H

AU - Schlüter, H

AU - Zidek, W

AU - Zimmermann, N

AU - Schmitz, W

PY - 1999/2

Y1 - 1999/2

N2 - Diadenosine tetraphosphate (AP4A) is an endogenous compound and exerts diverse physiological effects in animal systems. However, the effects of AP4A on inotropy in ventricular cardiac preparations have not yet been studied. The effects of AP4A on force of contraction (FOC) were studied in isolated electrically driven guinea pig and human cardiac preparations. Furthermore, the effects of AP4A on L-type calcium current and [Ca]i were studied in isolated guinea pig ventricular myocytes. In guinea pig left atria, AP4A (0.1-100 microM) reduced FOC maximally by 36.5 +/- 4.3%. In guinea pig papillary muscles, AP4A (100 microM) alone was ineffective, but reduced isoproterenol-stimulated FOC maximally by 29.3 +/- 3.4%. The negative inotropic effects of AP4A in atria and papillary muscles were abolished by the A1-adenosine receptor antagonist 1, 3-dipropyl-cyclopentylxanthine. In guinea pig ventricular myocytes, AP4A (100 microM) attenuated isoproterenol-stimulated L-type calcium current and [Ca]i. In human atrial and ventricular preparations, AP4A (100 microM) alone increased FOC to 158.3 +/- 12.4% and 167.5 +/- 25.1%, respectively. These positive inotropic effects were abolished by the P2-purinoceptor antagonist suramin. On the other hand, AP4A (100 microM) reduced FOC by 27.2 +/- 7.4% in isoproterenol-stimulated human ventricular trabeculae. The latter effect was abolished by 1,3-dipropyl-cyclopentylxanthine. In summary, after beta adrenergic stimulation AP4A exerts negative inotropic effects in animal and human ventricular preparations via stimulation of A1-adenosine receptors. In contrast, AP4A alone can exert positive inotropic effects via P2-purinoceptors in human ventricular myocardium. Thus, P2-purinoceptor stimulation might be a new positive inotropic principle in the human myocardium.

AB - Diadenosine tetraphosphate (AP4A) is an endogenous compound and exerts diverse physiological effects in animal systems. However, the effects of AP4A on inotropy in ventricular cardiac preparations have not yet been studied. The effects of AP4A on force of contraction (FOC) were studied in isolated electrically driven guinea pig and human cardiac preparations. Furthermore, the effects of AP4A on L-type calcium current and [Ca]i were studied in isolated guinea pig ventricular myocytes. In guinea pig left atria, AP4A (0.1-100 microM) reduced FOC maximally by 36.5 +/- 4.3%. In guinea pig papillary muscles, AP4A (100 microM) alone was ineffective, but reduced isoproterenol-stimulated FOC maximally by 29.3 +/- 3.4%. The negative inotropic effects of AP4A in atria and papillary muscles were abolished by the A1-adenosine receptor antagonist 1, 3-dipropyl-cyclopentylxanthine. In guinea pig ventricular myocytes, AP4A (100 microM) attenuated isoproterenol-stimulated L-type calcium current and [Ca]i. In human atrial and ventricular preparations, AP4A (100 microM) alone increased FOC to 158.3 +/- 12.4% and 167.5 +/- 25.1%, respectively. These positive inotropic effects were abolished by the P2-purinoceptor antagonist suramin. On the other hand, AP4A (100 microM) reduced FOC by 27.2 +/- 7.4% in isoproterenol-stimulated human ventricular trabeculae. The latter effect was abolished by 1,3-dipropyl-cyclopentylxanthine. In summary, after beta adrenergic stimulation AP4A exerts negative inotropic effects in animal and human ventricular preparations via stimulation of A1-adenosine receptors. In contrast, AP4A alone can exert positive inotropic effects via P2-purinoceptors in human ventricular myocardium. Thus, P2-purinoceptor stimulation might be a new positive inotropic principle in the human myocardium.

KW - Animals

KW - Calcium

KW - Calcium Channels

KW - Cells, Cultured

KW - Dinucleoside Phosphates

KW - Drug Interactions

KW - Guinea Pigs

KW - Heart

KW - Heart Atria

KW - Heart Ventricles

KW - Humans

KW - In Vitro Techniques

KW - Male

KW - Myocardial Contraction

KW - Myocardium

KW - Platelet Aggregation Inhibitors

KW - Xanthines

KW - Comparative Study

KW - Journal Article

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

M3 - SCORING: Journal article

C2 - 9918592

VL - 288

SP - 805

EP - 813

JO - J PHARMACOL EXP THER

JF - J PHARMACOL EXP THER

SN - 0022-3565

IS - 2

ER -