IP3 receptor-dependent Ca2+ release modulates excitation-contraction coupling in rabbit ventricular myocytes

2008 ◽  
Vol 294 (2) ◽  
pp. H596-H604 ◽  
Author(s):  
Timothy L. Domeier ◽  
Aleksey V. Zima ◽  
Joshua T. Maxwell ◽  
Sabine Huke ◽  
Gregory A. Mignery ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Ventricular Myocardium ◽  
Ip3 Receptor ◽  
Inotropic Effects ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rabbit Ventricular Myocytes ◽  
Receptor Clusters ◽  
Type 3

Inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-dependent Ca2+ signaling exerts positive inotropic, but also arrhythmogenic, effects on excitation-contraction coupling (ECC) in the atrial myocardium. The role of IP3R-dependent sarcoplasmic reticulum (SR) Ca2+ release in ECC in the ventricular myocardium remains controversial. Here we investigated the role of this signaling pathway during ECC in isolated rabbit ventricular myocytes. Immunoblotting of proteins from ventricular myocytes showed expression of both type 2 and type 3 IP3R at levels ∼3.5-fold less than in atrial myocytes. In permeabilized myocytes, direct application of IP3 (10 μM) produced a transient 21% increase in the frequency of Ca2+ sparks ( P < 0.05). This increase was accompanied by a 13% decrease in spark amplitude ( P < 0.05) and a 7% decrease in SR Ca2+ load ( P < 0.05) and was inhibited by IP3R antagonists 2-aminoethoxydiphenylborate (2-APB; 20 μM) and heparin (0.5 mg/ml). In intact myocytes endothelin-1 (100 nM) was used to stimulate IP3 production and caused a 38% ( P < 0.05) increase in the amplitude of action potential-induced (0.5 Hz, field stimulation) Ca2+ transients. This effect was abolished by the IP3R antagonist 2-APB (2 μM) or by using adenoviral expression of an IP3 affinity trap that buffers cellular IP3. Together, these data suggest that in rabbit ventricular myocytes IP3R-dependent Ca2+ release has positive inotropic effects on ECC by facilitating Ca2+ release through ryanodine receptor clusters.

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
Gui-Rong Li ◽  
Min Zhang ◽  
Leslie S. Satin ◽  
Clive M. Baumgarten
Keyword(s):  
Action Potential ◽  
Cell Volume ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Current Clamp ◽  
Osmotic Swelling ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Fura 2 ◽  
Rabbit Ventricular Myocytes

We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current ( I Ca-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given I Ca-L, and later, both I Ca-L and the Ca2+ transient are inhibited.

Effects of Na+/Ca2+-exchanger Overexpression on Excitation–contraction Coupling in Adult Rabbit Ventricular Myocytes

2002 ◽  
Vol 34 (4) ◽  
pp. 389-400 ◽  
Author(s):  
Hardeep K. Ranu ◽  
Cesare M.N. Terracciano ◽  
Kerry Davia ◽  
Elena Bernobich ◽  
Babar Chaudhri ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Adult Rabbit ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rabbit Ventricular Myocytes

scholarly journals Subcellular [Ca2+]iGradients During Excitation-Contraction Coupling in Newborn Rabbit Ventricular Myocytes

1999 ◽  
Vol 85 (5) ◽  
pp. 415-427 ◽  
Author(s):  
Peter S. Haddock ◽  
William A. Coetzee ◽  
Emily Cho ◽  
Lisa Porter ◽  
Hideki Katoh ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Newborn Rabbit ◽  
Rabbit Ventricular Myocytes

scholarly journals Ryanodine Receptors Outside of Couplons are Involved in Excitation-Contraction Coupling in Rabbit Ventricular Myocytes

2010 ◽  
Vol 98 (3) ◽  
pp. 550a
Author(s):  
Natalia S. Torres ◽  
Eleonora Savio-Galimberti ◽  
Joshua I. Goldhaber ◽  
Christian Soeller ◽  
John H.B. Bridge ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rabbit Ventricular Myocytes

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

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