Why the study?
Does endothelial nitric oxide synthase (NOS3) mediate muscarinic regulation of beta-adrenergic L-type Ca2+ current in mouse ventricular myocytes?
Does endothelial nitric oxide synthase (NOS3) mediate muscarinic regulation of beta-adrenergic L-type Ca2+ current in mouse ventricular myocytes?
Nitric oxide generated by NOS3 is not required for muscarinic inhibition or rebound stimulation of beta-adrenergically regulated L-type Ca2+ current in ventricular myocytes.
No takes yet. Share an insight, caveat, or question.
NOS3 dispensable for muscarinic control of beta-adrenergic Ca current in mouse myocytes; leaves open its role in human ventricular physiology.
Belevych et al. (2000) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: