Role of Potassium Currents in the Formation of After-Hyperpolarization Phase of Extracellular Action Potentials Recorded from the Control and Diabetic Rat Heart Ventricular Myocytes

2021 ◽  
Vol 57 (6) ◽  
pp. 1511-1521
Author(s):  
I. V. Kubasov ◽  
A. V. Stepanov ◽  
A. A. Panov ◽  
O. V. Chistyakova ◽  
I. B. Sukhov ◽  
...  
2010 ◽  
Vol 9 (1) ◽  
pp. 39 ◽  
Author(s):  
Ru-xing Wang ◽  
Xiao-rong Li ◽  
Tao Guo ◽  
Li-ping Sun ◽  
Su-xia Guo ◽  
...  

1999 ◽  
Vol 77 (6) ◽  
pp. 383-397
Author(s):  
Qi-Ying Liu ◽  
Mario Vassalle

The role of Na-Ca exchange in the membrane potential changes caused by repetitive activity ("drive") was studied in guinea pig single ventricular myocytes exposed to different [Ca2+]o. The following results were obtained. (i) In 5.4 mM [Ca2+]o, the action potentials (APs) gradually shortened during drive, and the outward current during a train of depolarizing voltage clamp steps gradually increased. (ii) The APs shortened more and were followed by a decaying voltage tail during drive in the presence of 5 mM caffeine; the outward current became larger and there was an inward tail current on repolarization during a train of depolarizing steps. (iii) These effects outlasted drive so that immediately after a train of APs, currents were already bigger and, after a train of steps, APs were already shorter. (iv) In 0.54 mM [Ca2+]o, the above effects were much smaller. (v) In high [Ca2+]o APs were shorter and outward currents larger than in low [Ca2+]o. (vi) In 10.8 mM [Ca2+]o, both outward and inward currents during long steps were exaggerated by prior drive, even with steps (+80 and +120 mV) at which there was no apparent inward current identifiable as ICa. (vii) In 0.54 mM [Ca2+]o, the time-dependent outward current was small and prior drive slightly increased it. (viii) During long steps, caffeine markedly increased outward and inward tail currents, and these effects were greatly decreased by low [Ca2+]o. (ix) After drive in the presence of caffeine, Ni2+ decreased the outward and inward tail currents. It is concluded that in the presence of high [Ca2+]o drive activates outward and inward Na-Ca exchange currents. During drive, the outward current participates in the plateau shortening and the inward tail current in the voltage tail after the action potential.Key words: ventricular myocytes, repetitive activity, outward and inward Na-Ca exchange currents, caffeine, nickel.


2007 ◽  
Vol 42 (6) ◽  
pp. S26
Author(s):  
Ayca Bilginoglu ◽  
Figen Amber ◽  
Mehmet Ugur ◽  
Hakan Gurdal ◽  
Belma Turan

2007 ◽  
Vol 305 (1-2) ◽  
pp. 63-69 ◽  
Author(s):  
Ayca Bilginoglu ◽  
Figen Amber Cicek ◽  
Mehmet Ugur ◽  
Hakan Gurdal ◽  
Belma Turan

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Toru Okazaki ◽  
Hajime Otani ◽  
Koji Yamashita ◽  
Hiromi Jo ◽  
Kei Yoshioka ◽  
...  

Although expression of inducible nitric oxide synthase (iNOS) and oxidative stress are increased in diabetic (DM) hearts, the role of iNOS uncoupling in ischemia/reperfusion (IR) injury remains unknown. Because iNOS-derived NO is known to play a crucial role in cardioprotection against IR injury in non-DM hearts, we hypothesized that iNOS uncoupling may compromise tolerance to IR injury in the DM heart by decreasing the bioavailability of NO. The expression and activity of iNOS but not n/eNOS were increased in the streptozotocin-induced DM rat heart. Under Langendorff perfusion, superoxide generation as evaluated by dihydroethidium accumulation in the nucleus was significantly increased in cardiomyocytes of the DM heart, but it was inhibited by treatment with the NOS co-factor tetrahydrobiopterin (BH4; 10 μM) or an iNOS selective inhibitor 1400W (10 μM). BH4 increased NOx, a marker of NO bioavailability, and cGMP in the DM heart. The increase in cGMP by BH4 was abrogated by co-treatment with 1400W or a NO-sensitive guanylyl cyclase inhibitor ODQ (10 μM). BH4 significantly decreased nitrotyrosin formation but increased protein S -nitrosylation in the DM heart. The increase in protein S -nitrosylation by BH4 was abolished by co-treatment with a thiol reducing agent dithiothreitol (DTT; 5 mM). The isolated rat heart was subjected to 30 min global ischemia followed by 120 min reperfusion. Post-ischemic recovery of left ventricular (LV) function and infarct size was comparable between the non-DM and the DM hearts. Pre-ischemic treatment with BH4 significantly improved post-ischemic LV function and reduced infarct size only in the DM heart. Co-treatment with BH4 and 1400W, ODQ, or DTT had no significant effect on post-ischemic LV function and infarct size in the non-DM heart. However, co-treatment with BH4 and 1400W or DTT but not ODQ abolished BH4-induced improvement of post-ischemic LV function and reduction of infarct size in the DM heart. These results suggest that inhibition of iNOS uncoupling by BH4 confers cardioprotection against IR injury in the streptozotocin-induced DM rat heart by increasing the bioavailability of NO and this cardioprotective effect is mediated by protein S -nitrosylation but not cGMP.


2004 ◽  
pp. 78-85
Author(s):  
Yoshihiko Nishio ◽  
Akio Kanazawa ◽  
Yoshio Nagai ◽  
Hidetoshi Inagaki ◽  
Atsunori Kashiwagi

2004 ◽  
Vol 1011 (1) ◽  
pp. 78-85 ◽  
Author(s):  
YOSHIHIKO NISHIO ◽  
AKIO KANAZAWA ◽  
YOSHIO NAGAI ◽  
HIDETOSHI INAGAKI ◽  
ATSUNORI KASHIWAGI

1999 ◽  
Vol 277 (5) ◽  
pp. H1690-H1700 ◽  
Author(s):  
Susan E. Howlett ◽  
Wei Xiong ◽  
Cindy L. Mapplebeck ◽  
Gregory R. Ferrier

We investigated excitation-contraction (EC) coupling in isolated ventricular myocytes from prehypertrophic cardiomyopathic (CM) hamster hearts. Conventional and voltage-clamp recordings were made with high-resistance microelectrodes, and cell shortening was measured with a video-edge detector at 37°C. Contractions were depressed in myocytes from CM hearts, whether they were initiated by action potentials or voltage-clamp steps. As in guinea pig and rat, contraction in hamster myocytes could be triggered by a voltage-sensitive release mechanism (VSRM) or Ca2+-induced Ca2+ release (CICR). Selective activation of these mechanisms demonstrated that the defect in EC coupling was primarily caused by a defect in the VSRM. However, activation and inactivation properties of the VSRM were not altered. When the VSRM was inhibited, the remaining contractions induced by CICR exhibited identical bell-shaped contraction voltage relations in normal and CM myocytes. Inward Ca2+current was unchanged. Thus a defect in the VSRM component of EC coupling precedes the development of hypertrophy and failure in CM hamster heart.


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