Key result
Cardiac CFTR chloride channels are activated by beta-adrenergic stimulation via the cyclic AMP/PKA pathway and inhibited by alpha-1-adrenergic agonists, endothelin-1, and angiotensin-II.
The complex hormonal regulation of cardiac CFTR chloride channels modulates action potential duration, which may play a significant role in arrhythmogenesis and autonomic regulation of the heart.
The chloride conductance that arises from the stimulation of beta-adrenoceptors has been shown to be carried by a cardiac isoform of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels. This brief review will focus first upon the cellular signal transduction system for the activation of this type of Cl- channels and then its regulation by catecholamines, muscarinic agonists, endothelin-1 and angiotensin-II. Both in physiological and pathological conditions, the complex interaction of these agonists modulates the Cl- conductance, which is potentially arrhythmogenic by shortening the action potential duration and inducing the depolarization.
No takes yet. Share an insight, caveat, or question.
Horie et al. (1996) conducted a review in Cardiac electrophysiology. Hormonal modulation was evaluated. Cardiac CFTR chloride channels are activated by beta-adrenergic stimulation via the cyclic AMP/PKA pathway and inhibited by alpha-1-adrenergic agonists, endothelin-1, and angiotensin-II.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: