scholarly journals Action potential shortening rescues atrial calcium alternans

2018 ◽  
Vol 597 (3) ◽  
pp. 723-740 ◽  
Author(s):  
Giedrius Kanaporis ◽  
Zane M. Kalik ◽  
Lothar A. Blatter
Keyword(s):  
Action Potential ◽  
Action Potential Shortening

ROLE OF ACTION POTENTIAL SHORTENING IN THE PREVENTION OF ARRHYTHMIAS IN CANINE CARDIAC TISSUE

1999 ◽  
Vol 26 (12) ◽  
pp. 964-969 ◽  
Author(s):  
Kawonia P Mull ◽  
Qadriyyah Debnam ◽  
Syeda M Kabir ◽  
Mohit Lal Bhattacharyya
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Action Potential Shortening

Time course of postnatal changes in rat heart action potential and in transient outward current is different

1994 ◽  
Vol 267 (3) ◽  
pp. H1157-H1166 ◽  
Author(s):  
G. M. Wahler ◽  
S. J. Dollinger ◽  
J. M. Smith ◽  
K. L. Flemal
Keyword(s):  
Action Potential ◽  
Rat Heart ◽  
Action Potentials ◽  
Time Course ◽  
Outward Current ◽  
Transient Outward Current ◽  
Papillary Muscles ◽  
Isolated Cells ◽  
Time Courses ◽  
Action Potential Shortening

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito. In 8- to 10-day muscles, 4-AP caused a small, but significant, increase in APD25. Ito increased slightly between day 1 and days 8-10, but this increase was not significant. Most of the increase in Ito (79%) and in the response to 4-AP (64%) occurred between days 8-10 and adult; however, approximately 75% of the APD25 shortening took place by days 8-10. Thus, while Ito may contribute to repolarization in late neonatal and adult cells, the different time courses of action potential shortening and increases in Ito suggest that changes in Ito are unlikely to be responsible for most of the postnatal action potential shortening.

Effects of ACh and adenosine mediated by Kir3.1 and Kir3.4 on ferret ventricular cells

2002 ◽  
Vol 283 (2) ◽  
pp. H615-H630 ◽  
Author(s):  
H. Dobrzynski ◽  
N. C. Janvier ◽  
R. Leach ◽  
J. B. C. Findlay ◽  
M. R. Boyett
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Current Clamp ◽  
Inotropic Effects ◽  
Clamp Technique ◽  
Action Potential Clamp ◽  
Ventricular Cells ◽  
Action Potential Waveform ◽  
Potential Waveform ◽  
Action Potential Shortening

The inotropic effects of ACh and adenosine on ferret ventricular cells were investigated with the action potential-clamp technique. Under current clamp, both agonists resulted in action potential shortening and a decrease in contraction. Under action potential clamp, both agonists failed to decrease contraction substantially. In the absence of agonist, application of the short action potential waveform (recorded previously in the presence of agonist) also resulted in a decrease in contraction. Under action potential clamp, application of ACh resulted in a Ba2+-sensitive outward current with the characteristics of muscarinic K+ current ( I K,ACh); the presence of the muscarinic K+ channel was confirmed by PCR and immunocytochemistry. In the absence of agonist, on application of the short ACh action potential waveform, the decrease in contraction was accompanied by loss of the inward Na+/Ca2+exchange current ( I NaCa). ACh also inhibited the background inward K+ current ( I K,1). It is concluded that ACh activates I K,ACh, inhibits I K,1, and indirectly inhibits I NaCa; this results in action potential shortening, decrease in contraction, and, as a result of the inhibition of I K,1, minimum decrease in excitability.

scholarly journals P133Atrial fibrillation vulnerability and action potential shortening in high fat diet-induced obesity in mice

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S34-S34
Author(s):  
V Galand ◽  
N Mougenot ◽  
A Coulombe ◽  
N Suffee-Mosbah ◽  
N Doisne ◽  
...  
Keyword(s):  
Action Potential ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity In Mice ◽  
Action Potential Shortening

Functional Modulation of Cardiac ATP-Sensitive K+ Channels

Physiology ◽  
1998 ◽  
Vol 13 (3) ◽  
pp. 131-137 ◽  
Author(s):  
Masayasu Hiraoka ◽  
Tetsushi Furukawa
Keyword(s):  
Action Potential ◽  
Channel Activity ◽  
K Channels ◽  
Channel Function ◽  
Intracellular Atp ◽  
Functional Modulation ◽  
Action Potential Shortening

ATP-sensitive K+ (KATP) channels are inhibited by intracellular ATP, but MgATP is necessary to maintain the channel activity. Numerous cofactors modulate channel function. K+ channel openers activate and sulfonylureas inhibit KATP channels. The structure of cardiac KATP channel is a complex of mainly KIR6.2 and SUR2a. Activation of cardiac KATP channels contributes to action potential shortening during ischemia and plays a role in cardioprotection.

Mechanism of atrioventricular nodal facilitation in the rabbit heart: role of the distal AV node

1997 ◽  
Vol 272 (6) ◽  
pp. H2815-H2825 ◽  
Author(s):  
G. J. Fahy ◽  
I. Efimov ◽  
Y. Cheng ◽  
G. A. Kidwell ◽  
D. Van Wagoner ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Cellular Response ◽  
Rabbit Heart ◽  
Av Node ◽  
Microelectrode Recordings ◽  
Bundle Of His ◽  
Action Potential Shortening

We investigated whether atrioventricular (AV) nodal facilitation is the result of distal AV nodal action potential shortening. Atrial and bundle of His (H) electrograms and microelectrode recordings from proximal and distal AV nodal cells were analyzed in eight superfused rabbit AV node preparations in response to two pacing protocols. In the facilitation protocol, an atrial extrastimulus (A3) was preceded by an atrial impulse (A2) introduced 300, 200, 150, or 125 ms after 30 basic beats (A1). The preexcitation protocol differed from the facilitation protocol by the addition of a premature His depolarization (h2) such that the H1-h2 interval was shorter than the H1-H2 interval. Conduction curves (A3-H3 vs. H2-A3, h2-A3, and A2-A3 intervals) were constructed. Facilitation was demonstrated in all preparations when H2-A3 was used (P = 0.02) but not in the A2-A3 format. Compared with facilitation at the same A1-A2 intervals, preexcitation, despite shortening the distal cellular action potential duration, resulted in longer A3-H3 delays (P = 0.002), shorter A2-A3 intervals, and depression of the proximal nodal cellular response. Thus facilitation does not result from altered distal AV nodal characteristics and instead is a manifestation of an uncontrolled pacing protocol-dependent modulation of proximal AV nodal function.

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