Key result
Although muscarinic constitutive inhibition of adenylyl cyclase is increased in heart failure, it does not contribute to the reduced beta-adrenoceptor-mediated inotropic effects in rat ventricles.
Why the study?
Does blockade of muscarinic receptors or inactivation of Gi protein modify cAMP-dependent inotropic effects in failing rat ventricle?
Population
Rat ventricle with post-infarction heart failure (HF) and sham-operated (Sham) controls
Comparison
Blockade of muscarinic receptors by atropine and… vs Sham-operated controls with or without blockade
Design
Preclinical
Authors
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No support for muscarinic blockade to restore beta-inotropy in rat HF; leaves open mechanisms in human ventricle.
Does blockade of muscarinic receptors or inactivation of Gi protein modify cAMP-dependent inotropic effects in failing rat ventricle?
Muscarinic constitutive inhibition of adenylyl cyclase is increased in heart failure but does not contribute to reduced β-AR-mediated inotropic effects in rat ventricle.
Hussain et al. (2010) studied Heart failure. Atropine and pertussis toxin (PTX) vs. Sham-operated controls or no blockade was evaluated on Contractility and adenylyl cyclase (AC) activity. Although muscarinic constitutive inhibition of adenylyl cyclase is increased in heart failure, it does not contribute to the reduced beta-adrenoceptor-mediated inotropic effects in rat ventricles.
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