scholarly journals Inhibition of reverse‐mode sodium‐calcium exchange by the anti‐anginal agent ranolazine.

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Daniel Soliman ◽  
Liango Wang ◽  
Kevin SC Hamming ◽  
Laura C Matemisz ◽  
Alexander S Clanachan ◽  
...  
Keyword(s):  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange

scholarly journals Role of reverse‐mode sodium‐calcium exchange to serotonergic contractility in pulmonary arteries of hypoxic sheep

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Ravi Goyal ◽  
Dan Nguyen ◽  
William J Pearce ◽  
Lawrence D Longo ◽  
Sean M Wilson
Keyword(s):  
Pulmonary Arteries ◽  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange

scholarly journals Contribution of reverse-mode sodium–calcium exchange to contractions in failing human left ventricular myocytes

1998 ◽  
Vol 37 (2) ◽  
pp. 424-431 ◽  
Author(s):  
Julian A Mattiello ◽  
Kenneth B Margulies ◽  
Valluvan Jeevanandam ◽  
Steven R Houser
Keyword(s):  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange

Sodium-calcium exchange-mediated contractions in feline ventricular myocytes

1992 ◽  
Vol 263 (4) ◽  
pp. H1161-H1169 ◽  
Author(s):  
H. B. Nuss ◽  
S. R. Houser
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Membrane Potentials ◽  
Exchange Mechanism ◽  
Ca Channel ◽  
Ca Current ◽  
Voltage Step ◽  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange

The hypothesis that Ca entry by the sarcolemmal Na-Ca exchange mechanism induces sarcoplasmic reticulum (SR) Ca release, loads the SR with Ca, and/or directly induces contractions by elevating cytosolic free Ca was tested in voltage-clamped feline ventricular myocytes. Intracellular Na concentration was increased by cellular dialysis to enhance Ca influx via "reverse-mode" Na-Ca exchange at positive membrane potentials, at which the "L-type" Ca current (ICa) should be small. Contractions were induced in the presence of Ca channel antagonists by depolarization to these potentials, suggesting that Ca influx via reverse-mode Na-Ca exchange was involved. These contractions had both phasic (SR related) and tonic components of shortening. They were smaller and began with more delay after depolarization than contractions which involved ICa. The magnitude of shortening was graded by the amount and duration of depolarization, suggesting that Ca influx via reverse-mode Na-Ca exchange has the capacity to induce and grade SR Ca release. Small slow contractions could be evoked in the presence of ryanodine (to impair SR function) and verapamil (to block ICa), supporting the idea that Ca influx via Na-Ca exchange is sufficient to directly activate the contractile proteins. Contractions induced by voltage steps to +10 mV, which were usually small when ICa was blocked, were potentiated if preceded by a voltage step to strongly positive potentials. This potentiation was inhibited by ryanodine, suggesting that Ca entry that occurs by Na-Ca exchange may be important for normal SR Ca loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular Regulation of Sodium-Calcium Exchange

2006 ◽  
Vol 976 (1) ◽  
pp. 214-223 ◽  
Author(s):  
MADALINA CONDRESCU ◽  
KWABENA OPUNI ◽  
BASIL M. HANTASH ◽  
JOHN P. REEVES
Keyword(s):  
Cellular Regulation ◽  
Sodium Calcium ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange
Sign in / Sign up

Export Citation Format

Share Document