Reduction of [Ca2+]i restores uncoupled β-adrenergic signaling in isolated perfused transgenic mouse hearts

Circulation Research

Volumn 88, Issue 1, 2001, Pages 9-11

  Serikov, Vladimir B ^a   Petrashevskaya, Natalia N ^a   Canning, Amy M ^a   Schwartz, Arnold ^a,b  

^a UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

^b UNIVERSITY OF CINCINNATI   (United States)

Author keywords

Adenylyl cyclase; Calcium; Cardiac hypertrophy

Indexed keywords

BETA ADRENERGIC RECEPTOR STIMULATING AGENT;

ANIMAL TISSUE; ARTICLE; BETA ADRENERGIC STIMULATION; CALCIUM TRANSPORT; HEART CONTRACTION; HEART MUSCLE CONTRACTILITY; MOUSE; NONHUMAN; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

EID: 0035910616     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.88.1.9     Document Type: Article

References (11)

1. Screening of inotropic drugs in isolated rat and guinea pig hearts
2. Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of β-agonist stimulation
3. Single adult rabbit and rat cardiac myocytes retain the Ca and species-dependent systolic and diastolic contractile properties of intact muscle
4. Calcium fluxes involved in control of cardiac myocyte contraction
5. Calcium cycling and contractile activation in intact mouse cardiac muscle
6. q mediated cardiac hypertrophy and ventricular dysfunction
7. 2+-dependent transgenic model of cardiac hypertrophy: A role of PKCα
8. Functional consequences of altering myocardial adrenergic receptor signaling
9. Co-regulation of calcium channels and β-adrenergic receptors in cultured chick-embryo ventricular cells
10. Adenylyl cyclases and the interaction between calcium and cAMP signaling
11. Cardiac-specific overexpression of Gαq alters excitation-contraction coupling in isolated cardiac myocytes