scholarly journals Action Potential Prolongation, β-Adrenergic Stimulation, and Angiotensin II as Co-factors in Sarcoplasmic Reticulum Instability

2019 ◽  
Vol 9 ◽  
Author(s):  
Carlotta Ronchi ◽  
Beatrice Badone ◽  
Joyce Bernardi ◽  
Antonio Zaza
Keyword(s):  
Angiotensin Ii ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Adrenergic Stimulation ◽  
Action Potential Prolongation

Increased ICaL Underlies Ventricular Action-Potential Prolongation After Spontaneous Ca2+ Release From The Sarcoplasmic Reticulum

Heart Rhythm ◽  
2011 ◽  
Vol 8 (11) ◽  
pp. 1823 ◽  
Author(s):  
D.M. Johnson ◽  
J. Heijman ◽  
E.F. Bode ◽  
D.J. Greensmith ◽  
N. Abi-Gerges ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Action Potential Prolongation ◽  
Ventricular Action Potential

Electrophysiological effects of alpha 2-adrenergic stimulation in canine cardiac Purkinje fibers

1995 ◽  
Vol 268 (5) ◽  
pp. H2024-H2035 ◽  
Author(s):  
R. A. Samson ◽  
J. J. Cai ◽  
E. F. Shibata ◽  
J. B. Martins ◽  
H. C. Lee
Keyword(s):  
Action Potential ◽  
Pertussis Toxin ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Action Potential Prolongation ◽  
Delayed Afterdepolarizations ◽  
Baseline Values ◽  
Electrophysiological Effects

The effects of alpha 2-adrenergic stimulation on action potentials were measured in isolated canine Purkinje fibers. Action potential durations at 50 and 90% of repolarization (APD50 and APD90) were significantly prolonged by 0.25 microM l-norepinephrine + 0.5 microM dl-propranolol (NE+P) from baseline values of 166 +/- 7 and 249 +/- 9 (SE) ms (n = 7) to 174 +/- 7 and 265 +/- 9 ms, respectively (P < 0.05 for both). Selective alpha 2-blockade with 0.01 microM yohimbine (YO) reduced this prolongation by NE+P in APD50 and APD90 to 169 +/- 7 and 256 +/- 8 ms, respectively (P < 0.05 compared with NE+P). Additional selective alpha 1-blockade with 0.01 microM prazosin (PZ) completely blocked the effects of NE+P, returning APD50 and APD90 to 163 +/- 7 and 250 +/- 9 ms (not different from baseline). After incubation of isolated Purkinje fibers with pertussis toxin (1 microgram/ml), which reduced the availability of a 41-kDa membrane protein for ADP ribosylation by 70 +/- 7% (n = 4, P < 0.05), YO failed to reverse the prolongation in action potential durations brought on by NE+P, but the effects of PZ were intact. The effects of alpha 2-stimulation on beta-adrenergic-induced delayed afterdepolarizations (DADs) were studied by burst pacing of Purkinje fibers in Tyrode solution containing 7.5 mM Ca2+. The DADs induced in the presence of NE+PZ (beta- + alpha 2-stimulation) were significantly smaller in amplitude and required a shorter pacing cycle length to reach threshold than those induced in the presence of NE+PZ+YO (unopposed beta-adrenergic stimulation). Furthermore sustained triggered activity, seen in five of eight preparations under beta-stimulation, could no longer be elicited in the presence of beta- + alpha 2-stimulation. These results suggest that the postjunctional alpha 2-adrenergic receptors in canine Purkinje fibers are coupled to a pertussis toxin-sensitive G protein and that stimulation of these receptors leads to action potential prolongation and suppression of DADs induced by beta-adrenergic stimulation.

Valsartan reduced the vulnerability to atrial fibrillation by preventing action potential prolongation and conduction slowing in castrated male mice

2018 ◽  
Vol 29 (10) ◽  
pp. 1436-1443 ◽  
Author(s):  
Yi-Lin Sun ◽  
Peng-Hui Li ◽  
Ling Shi ◽  
Wan-Zhen Su ◽  
De-Sheng Li ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Male Mice ◽  
Action Potential Prolongation

scholarly journals cAMP-dependent regulation of IKs single-channel kinetics

2017 ◽  
Vol 149 (8) ◽  
pp. 781-798 ◽  
Author(s):  
Emely Thompson ◽  
Jodene Eldstrom ◽  
Maartje Westhoff ◽  
Donald McAfee ◽  
Elise Balse ◽  
...  
Keyword(s):  
Action Potential ◽  
Single Channel ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Surface Expression ◽  
Voltage Sensor ◽  
Single Channels ◽  
Adrenergic Stimulation ◽  
Channel Opening ◽  
Sensor Activation

The delayed potassium rectifier current, IKs, is composed of KCNQ1 and KCNE1 subunits and plays an important role in cardiac action potential repolarization. During β-adrenergic stimulation, 3′-5′-cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) phosphorylates KCNQ1, producing an increase in IKs current and a shortening of the action potential. Here, using cell-attached macropatches and single-channel recordings, we investigate the microscopic mechanisms underlying the cAMP-dependent increase in IKs current. A membrane-permeable cAMP analog, 8-(4-chlorophenylthio)-cAMP (8-CPT-cAMP), causes a marked leftward shift of the conductance–voltage relation in macropatches, with or without an increase in current size. Single channels exhibit fewer silent sweeps, reduced first latency to opening (control, 1.61 ± 0.13 s; cAMP, 1.06 ± 0.11 s), and increased higher-subconductance-level occupancy in the presence of cAMP. The E160R/R237E and S209F KCNQ1 mutants, which show fixed and enhanced voltage sensor activation, respectively, largely abolish the effect of cAMP. The phosphomimetic KCNQ1 mutations, S27D and S27D/S92D, are much less and not at all responsive, respectively, to the effects of PKA phosphorylation (first latency of S27D + KCNE1 channels: control, 1.81 ± 0.1 s; 8-CPT-cAMP, 1.44 ± 0.1 s, P &lt; 0.05; latency of S27D/S92D + KCNE1: control, 1.62 ± 0.1 s; cAMP, 1.43 ± 0.1 s, nonsignificant). Using total internal reflection fluorescence microscopy, we find no overall increase in surface expression of the channel during exposure to 8-CPT-cAMP. Our data suggest that the cAMP-dependent increase in IKs current is caused by an increase in the likelihood of channel opening, combined with faster openings and greater occupancy of higher subconductance levels, and is mediated by enhanced voltage sensor activation.

scholarly journals Spontaneous calcium release in tissue from the failing canine heart

2009 ◽  
Vol 297 (4) ◽  
pp. H1235-H1242 ◽  
Author(s):  
Gregory S. Hoeker ◽  
Rodolphe P. Katra ◽  
Lance D. Wilson ◽  
Bradley N. Plummer ◽  
Kenneth R. Laurita
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Tissue Level ◽  
Calcium Handling ◽  
Canine Heart ◽  
Myocardial Cells ◽  
Spontaneous Release ◽  
Adrenergic Stimulation ◽  
Electrical Instability ◽  
Delayed Afterdepolarization

Abnormalities in calcium handling have been implicated as a significant source of electrical instability in heart failure (HF). While these abnormalities have been investigated extensively in isolated myocytes, how they manifest at the tissue level and trigger arrhythmias is not clear. We hypothesize that in HF, triggered activity (TA) is due to spontaneous calcium release from the sarcoplasmic reticulum that occurs in an aggregate of myocardial cells (an SRC) and that peak SCR amplitude is what determines whether TA will occur. Calcium and voltage optical mapping was performed in ventricular wedge preparations from canines with and without tachycardia-induced HF. In HF, steady-state calcium transients have reduced amplitude [135 vs. 170 ratiometric units (RU), P < 0.05] and increased duration (252 vs. 229 s, P < 0.05) compared with those of normal. Under control conditions and during β-adrenergic stimulation, TA was more frequent in HF (53% and 93%, respectively) compared with normal (0% and 55%, respectively, P < 0.025). The mechanism of arrhythmias was SCRs, leading to delayed afterdepolarization-mediated triggered beats. Interestingly, the rate of SCR rise was greater for events that triggered a beat (0.41 RU/ms) compared with those that did not (0.18 RU/ms, P < 0.001). In contrast, there was no difference in SCR amplitude between the two groups. In conclusion, TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the sarcoplasmic reticulum in aggregates of myocardial cells (i.e., an SCR), but importantly, it is the rate of SCR rise rather than amplitude that was associated with TA.

scholarly journals Action potential contour contributes to species differences in repolarization response to β-adrenergic stimulation

EP Europace ◽  
2017 ◽  
Vol 20 (9) ◽  
pp. 1543-1552 ◽  
Author(s):  
Luca Sala ◽  
Bence Hegyi ◽  
Chiara Bartolucci ◽  
Claudia Altomare ◽  
Marcella Rocchetti ◽  
...  
Keyword(s):  
Action Potential ◽  
Species Differences ◽  
Adrenergic Stimulation

Relation between contractile function and regulatory cardiac proteins in hypertrophied hearts

1996 ◽  
Vol 270 (6) ◽  
pp. H2021-H2028 ◽  
Author(s):  
B. Stein ◽  
S. Bartel ◽  
U. Kirchhefer ◽  
S. Kokott ◽  
E. G. Krause ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Troponin I ◽  
Contractile Function ◽  
Papillary Muscles ◽  
Camp Accumulation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
C Protein ◽  
Camp Formation ◽  
Phosphate Incorporation

The aim of this study was to examine the mechanism(s) underlying the reduced isoproterenol-induced positive inotropic and lusitropic effects in hypertrophied hearts. Chronic beta-adrenergic stimulation (2.4 mg isoproterenol.kg-1. day-1 for 4 days) induced cardiac hypertrophy by 33 +/- 2% in rats. A parallel downregulation of phospholamban (PLB) and sarcoplasmic reticulum Ca2(+)-ATPase (SERCA2) protein expression by 49 and 40%, respectively, was observed, whereas troponin I (TNI) and C protein remained unchanged. In papillary muscles from chronically beta-adrenergically stimulated rats, the isoproterenol-induced positive inotropic and lusitropic effects, as well as adenosine 3',5'-cyclic monophosphate (cAMP) accumulation, were attenuated compared with those in control animals. Acute exposure to isoproterenol induced phosphate incorporation into PLB, TNI, and C protein of 48 +/- 4.6, 55 +/- 5.0, and 27 +/- 4.9 pmol/mg homogenate protein, respectively, in control animals. In the hypertrophied hearts, phosphate incorporation into PLB was reduced by 76%, whereas phosphate incorporation into TNI or C protein remained unchanged. In conclusion, chronic beta-adrenergic stimulation reduced the isoproterenol-stimulated positive inotropic and lusitropic effects in papillary muscles, which were accompanied by 1) diminished cAMP formation, 2) attenuation of cAMP-mediated PLB phosphorylation, and 3) downregulation of PLB and SERCA2 protein.

scholarly journals Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2 + ATPase in atrial myocytes

2009 ◽  
Vol 10 (3) ◽  
pp. 121-126 ◽  
Author(s):  
Cho-Kai Wu ◽  
Chuen-Den Tseng ◽  
Yin-Tsen Huang ◽  
Chia-Shan Hsieh ◽  
Wei-Shan Tsai ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sarcoplasmic Reticulum ◽  
Atrial Myocytes
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