• Corpus ID: 92906067

Diurnal variation in excitation-contraction coupling in rat ventricular myocytes

  title={Diurnal variation in excitation-contraction coupling in rat ventricular myocytes},
  author={Helen E Collins},
Rodrigo, G.C., Collins, H.E. The role o f nitric oxide in the diumal variation in excitation-contraction coupling in ventricular myocytes. The Annual Physiological Society meeting, Dublin, July 2009. Poster presentation. Collins, H.E., Rodrigo, G.C. Diumal variation in excitation-contraction coupling in rat ventricular myocytes: sensitivity to P-adrenergic stimulation. The Annual Physiological Society meeting, Dublin, July 2009. Oral presentation. Collins, H.E., Rodrigo, G.C. Diumal variation… 



Inotropic Response of Cardiac Ventricular Myocytes to &bgr;-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation: Involvement of Nitric Oxide

The threshold for the development of arrhythmic activity in response to isoproterenol is higher during the active period of the rat, which is suggested to reflect a reduction in SR Ca2+ loading and a diurnal variation in neuronal NO synthase signaling.

CAPON modulates cardiac repolarization via neuronal nitric oxide synthase signaling in the heart

It is found that CAPON protein is expressed in the heart and interacts with NOS1 to accelerate cardiac repolarization by inhibition of L-type calcium channel, providing a rationale for the association of CAPON gene variants with extremes of the QT interval in human populations.

Cardiac Neuronal Nitric Oxide Synthase Isoform Regulates Myocardial Contraction and Calcium Handling

A novel mechanism by which intracellular Ca2+ is regulated in LV myocytes is uncovered and indicates that nNOS is an important determinant of basal contractility in the mammalian myocardium.

Role of cyclic GMP‐dependent protein kinase in the contractile response to exogenous nitric oxide in rat cardiac myocytes

The results suggest that the reduction in myofilament Ca2+ responsiveness produced by DEA/NO results from phosphorylation of troponin I by PKG, which is not attributable to an intracellular acidosis.

Nitric oxide and excitation-contraction coupling.

  • J. Hare
  • Biology
    Journal of molecular and cellular cardiology
  • 2003

Cardiac Nitric Oxide Synthase 1 Regulates Basal and &bgr;-Adrenergic Contractility in Murine Ventricular Myocytes

Findings indicate that cardiac NOS1-derived NO plays a significant role in the autocrine regulation of myocardial contractility and the inotropic response to &bgr;-adrenergic stimulation in murine ventricular myocytes.

Increased susceptibility to development of triggered activity in myocytes from mice with targeted disruption of endothelial nitric oxide synthase.

It is demonstrated that NO derived from myocyte eNOS activation suppresses ouabain-induced arrhythmic contractions by a mechanism that might involve activation of guanylyl cyclase and elevation of cGMP.

Nitric Oxide Regulation of Myocardial Contractility and Calcium Cycling: Independent Impact of Neuronal and Endothelial Nitric Oxide Synthases

There is NOS isoform-specific regulation of different facets of rate-dependent excitation-contraction coupling; inactivation of NOS1 has the potential to contribute to the pathophysiology of states characterized by diminished frequency-dependent inotropic responses.

Nitric oxide and cardiac function.

Future therapeutic manipulations of cardiac NO synthesis will necessarily draw on additional characterization of the cellular and molecular determinants for the net effect of this versatile radical on the cardiomyocyte biology.