scholarly journals 139 An investigation into the subcellular distribution of two-pore channels in cardiac ventricular myocytes in light of their differing contributions to beta-adrenergic signalling

Heart ◽  
2017 ◽  
Vol 103 (Suppl 5) ◽  
pp. A104-A105
Author(s):  
Hamish Jackson ◽  
Laura Elson ◽  
Stevan Rakovic
Keyword(s):  
Subcellular Distribution ◽  
Ventricular Myocytes ◽  
Beta Adrenergic ◽  
Cardiac Ventricular Myocytes

scholarly journals Dual role of junctin in the regulation of ryanodine receptors and calcium release in cardiac ventricular myocytes

2011 ◽  
Vol 589 (24) ◽  
pp. 6063-6080 ◽  
Author(s):  
Beth A. Altschafl ◽  
Demetrios A. Arvanitis ◽  
Oscar Fuentes ◽  
Qunying Yuan ◽  
Evangelia G. Kranias ◽  
...  
Keyword(s):  
Calcium Release ◽  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Dual Role ◽  
Cardiac Ventricular Myocytes

Opioid peptide receptor stimulation reverses beta-adrenergic effects in rat heart cells

1997 ◽  
Vol 272 (2) ◽  
pp. H797-H805 ◽  
Author(s):  
R. P. Xiao ◽  
S. Pepe ◽  
H. A. Spurgeon ◽  
M. C. Capogrossi ◽  
E. G. Lakatta
Keyword(s):  
Intracellular Signaling ◽  
Ventricular Myocytes ◽  
Opioid Peptide ◽  
Heart Cells ◽  
Beta Adrenergic ◽  
Inotropic Effects ◽  
Intracellular Signaling Pathway ◽  
Peptide Receptor ◽  
Cyclic Monophosphate ◽  
Adrenergic Effects

Opioid peptide receptor (OPR) agonists are co-released with the beta-adrenergic receptor (beta-AR) agonist norepinephrine (NE) from nerve terminals in the heart during sympathetic stimulation. Whereas recent studies indicate that OPR and beta-AR coexist on the surface of cardiac myocytes, whether significant "cross talk" occurs between OPR and beta-AR signaling cascades within heart cells is unknown. In the present study we demonstrate a marked effect of delta-OPR stimulation to modulate beta-adrenergic responses in single isolated rat ventricular myocytes. Nanomolar concentrations (10(-8) M) of the OPR agonist leucine enkephalin (LE), a naturally occurring delta-opioid peptide, inhibited NE-induced increases in sarcolemmal L-type Ca2+ current, cytosolic Ca2+ transient, and contraction. The antiadrenergic effect of LE was pertussis toxin sensitive and abolished by naloxone, an opioid receptor antagonist. In contrast, LE was unable to inhibit the positive inotropic effects induced by equipotent concentrations of 8-(4 chlorophenylthio)-adenosine 3',5'-cyclic monophosphate, a cell-permeant adenosine 3',5'-cyclic monophosphate analog, or by the non-receptor-induced increase in contraction by elevated bathing Ca2+ concentration. These results indicate that an interaction of the OPR and beta-AR systems occurs proximal to activation of the adenosine 3',5'-cyclic monophosphate-dependent protein kinase of the beta-AR intracellular signaling pathway. This modulation of beta-adrenergic effects by OPR activation at the myocyte level may have important implications in the regulation of cardiac Ca2+ metabolism and contractility, particularly during the myocardial response to stress.

scholarly journals Inhibitory effect of aprindine on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2002 ◽  
Vol 136 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Munekazu Shigekawa ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

Ca2+ mobilization by extracellular ATP in rat cardiac myocytes: regulation by protein kinase C and A

1992 ◽  
Vol 263 (5) ◽  
pp. C933-C940 ◽  
Author(s):  
J. S. Zheng ◽  
A. Christie ◽  
M. N. Levy ◽  
A. Scarpa
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ventricular Myocytes ◽  
Cell Voltage ◽  
Extracellular Atp ◽  
Camp Level ◽  
Intracellular Camp ◽  
Beta Adrenergic ◽  
Kinase C ◽  
Integrated Response

Activation of protein kinase C (PKC) modulates the mobilization of intracellular Ca2+ induced by extracellular ATP in rat ventricular myocytes. Pretreatment of myocytes with PKC activators attenuated both the ATP-induced Ca2+ transient and the noradrenergic potentiation of the Ca2+ response. Various PKC activators decreased both the basal cAMP level and the cAMP levels that had been elevated by norepinephrine, forskolin, or 3-isobutyl-1-methylxanthine. The inhibitory effects of PKC activators were reversed by the PKC inhibitor staurosporine. The ATP-induced Ca2+ response is an integrated response resulting from ATP eliciting an inward cation current (IATP), cellular depolarization, Ca2+ influx through Ca2+ channels, and Ca2+ release from the sarcoplasmic reticulum. We used the whole cell voltage-clamp technique to investigate which steps of this integrated response are affected by PKC. PKC activators did not significantly affect the IATP. In contrast, PKC activators decreased the basal Ca2+ current (ICa) or Ba2+ current and the beta-adrenergic-stimulated ICa. These results suggest that PKC-induced suppression of the ATP-induced Ca2+ response and the beta-adrenergic-potentiated Ca2+ response is achieved at least partially by decreasing the intracellular cAMP level and ICa.

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