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Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium.

Standard

Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium. / Janssen, Paul M L; Schillinger, Wolfgang; Donahue, J Kevin; Zeitz, Oliver; Emami, Shahriyar; Lehnart, Stephan E; Weil, Joachim; Eschenhagen, Thomas; Hasenfuss, Gerd; Prestle, Juergen.

in: CARDIOVASC RES, Jahrgang 55, Nr. 2, 2, 2002, S. 300-308.

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

Harvard

Janssen, PML, Schillinger, W, Donahue, JK, Zeitz, O, Emami, S, Lehnart, SE, Weil, J, Eschenhagen, T, Hasenfuss, G & Prestle, J 2002, 'Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium.', CARDIOVASC RES, Jg. 55, Nr. 2, 2, S. 300-308. <http://www.ncbi.nlm.nih.gov/pubmed/12123769?dopt=Citation>

APA

Janssen, P. M. L., Schillinger, W., Donahue, J. K., Zeitz, O., Emami, S., Lehnart, S. E., Weil, J., Eschenhagen, T., Hasenfuss, G., & Prestle, J. (2002). Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium. CARDIOVASC RES, 55(2), 300-308. [2]. http://www.ncbi.nlm.nih.gov/pubmed/12123769?dopt=Citation

Vancouver

Janssen PML, Schillinger W, Donahue JK, Zeitz O, Emami S, Lehnart SE et al. Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium. CARDIOVASC RES. 2002;55(2):300-308. 2.

Bibtex

@article{54b29546c4b2442eb93e5fec0fdb998f,
title = "Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium.",
abstract = "OBJECTIVE: Increased levels of inhibitory G proteins have been observed in heart failure, but their physiological relevance in mediating the reduced beta-adrenergic response is largely unknown. METHODS: To evaluate the functional consequences of Galpha(i2) overexpression, we studied myocardial contraction in intact isometric contracting cardiac rabbit trabeculae and isolated myocytes after adenovirus-mediated gene transfer of Galpha(i2). RESULTS: Neither Galpha(i2) nor lacZ (control) overexpression altered baseline contractile force. After 72 h of continuous contractions, developed force (F(dev)) increased after addition of 1 microM isoproterenol by 28.5+/-9.7 mN/mm(2) in the control group, which was unchanged from the initial response at t=0 h (23.7+/-3.8 mN/mm(2)). In sharp contrast, in preparations transfected with AdGalpha(i2), the response to isoproterenol was significantly attenuated (5.9+/-2.0 vs. 27.6+/-4.2 mN/mm(2), t=72 vs. 0 h, respectively, P",
author = "Janssen, {Paul M L} and Wolfgang Schillinger and Donahue, {J Kevin} and Oliver Zeitz and Shahriyar Emami and Lehnart, {Stephan E} and Joachim Weil and Thomas Eschenhagen and Gerd Hasenfuss and Juergen Prestle",
year = "2002",
language = "Deutsch",
volume = "55",
pages = "300--308",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium.

AU - Janssen, Paul M L

AU - Schillinger, Wolfgang

AU - Donahue, J Kevin

AU - Zeitz, Oliver

AU - Emami, Shahriyar

AU - Lehnart, Stephan E

AU - Weil, Joachim

AU - Eschenhagen, Thomas

AU - Hasenfuss, Gerd

AU - Prestle, Juergen

PY - 2002

Y1 - 2002

N2 - OBJECTIVE: Increased levels of inhibitory G proteins have been observed in heart failure, but their physiological relevance in mediating the reduced beta-adrenergic response is largely unknown. METHODS: To evaluate the functional consequences of Galpha(i2) overexpression, we studied myocardial contraction in intact isometric contracting cardiac rabbit trabeculae and isolated myocytes after adenovirus-mediated gene transfer of Galpha(i2). RESULTS: Neither Galpha(i2) nor lacZ (control) overexpression altered baseline contractile force. After 72 h of continuous contractions, developed force (F(dev)) increased after addition of 1 microM isoproterenol by 28.5+/-9.7 mN/mm(2) in the control group, which was unchanged from the initial response at t=0 h (23.7+/-3.8 mN/mm(2)). In sharp contrast, in preparations transfected with AdGalpha(i2), the response to isoproterenol was significantly attenuated (5.9+/-2.0 vs. 27.6+/-4.2 mN/mm(2), t=72 vs. 0 h, respectively, P

AB - OBJECTIVE: Increased levels of inhibitory G proteins have been observed in heart failure, but their physiological relevance in mediating the reduced beta-adrenergic response is largely unknown. METHODS: To evaluate the functional consequences of Galpha(i2) overexpression, we studied myocardial contraction in intact isometric contracting cardiac rabbit trabeculae and isolated myocytes after adenovirus-mediated gene transfer of Galpha(i2). RESULTS: Neither Galpha(i2) nor lacZ (control) overexpression altered baseline contractile force. After 72 h of continuous contractions, developed force (F(dev)) increased after addition of 1 microM isoproterenol by 28.5+/-9.7 mN/mm(2) in the control group, which was unchanged from the initial response at t=0 h (23.7+/-3.8 mN/mm(2)). In sharp contrast, in preparations transfected with AdGalpha(i2), the response to isoproterenol was significantly attenuated (5.9+/-2.0 vs. 27.6+/-4.2 mN/mm(2), t=72 vs. 0 h, respectively, P

M3 - SCORING: Zeitschriftenaufsatz

VL - 55

SP - 300

EP - 308

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 2

M1 - 2

ER -