The Role of Nitric Oxide in the Regulation of Mechanically Gated Channels in the Heart

Kazanski, Victor; Kamkin, Andre; Makarenko, E. Yu.; Lysenko, Natalia N.; Lapina, Natalia; Kiseleva, Irina

doi:10.1007/978-90-481-9881-8_5

Cited by 7 publications

(12 citation statements)

References 78 publications

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“…On the contrary, in cells from NOS3-/-mice stretch does not cause MG-current. The results discussed on the channel level testify to the NO role in activation and inactivation of MGCs in cardiomyocytes and demonstrate that NOS3 dominates as NO source (Kazanski et al, 2010b(Kazanski et al, , 2011. Therefore the appearance of hump-like SIDs and extra-AP during stretching of atrial tissue stripes is determined by MGCs functioning, which are modulated by NO and NO-synthases.…”

Section: Cytokines and Mechanosensitivity Of The Heartmentioning

confidence: 57%

“…Experimental data in this study was obtained from the isolated ventricular myocytes of mouse, rat and guinea pig by means of patch-clamp method in whole-cell configuration. The data demonstrated that NO donors lead to MGCs activation and appearance of MG-like currents in undeformed ventricular myocytes, whereas, it can also lead to the inactivation of the stretched cells with activation MGCs and inhibit the conductivity of these channels (Kazanski et al, 2010a(Kazanski et al, , 2011. NO scavenger PTIO causes inactivation of all MGCs.…”

Section: Cytokines and Mechanosensitivity Of The Heartmentioning

confidence: 89%

“…NO imparts cardiac effects via two general signaling modalities: (i) the activation of soluble guanylate cyclase and the formation of cGMP, which in turn activates protein kinase G (PKG) and PKG-dependent phosphorylation events; and (2) the direct oxidation of thiol residues on critical regulatory proteins (S-nitrosylation) (Kojda and Kottenberg, 1999;Prabhu, 2004a). Rise of intracellular NO concentration opens MGCs, which allows sodium entry into the cell which in turn depolarizes them, shifting resting membrane potential towards E C (Kazanski et al, 2011). This can directly or indirectly lead to arrhythmias triggered by elevated levels of cytokines.…”

Section: Discussionmentioning

confidence: 99%

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The Role of Proinflammatory Cytokines in Regulation of Cardiac Bioelectrical Activity: Link to Mechanoelectrical Feedback

Kuzmin¹,

Abramochkin²,

Mitrochin³

et al. 2011

Mechanical Stretch and Cytokines

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In this review we cover key issues, concerned with the effects of cytokines in cardiac tissue and cardiac cells. We discuss the effects of proinflammatory cytokines under non-pathological conditions and their mechanisms dependent and independent of nitric oxide. The role of proinflammatory cytokines is considered in acute myocardial infarction and in heart failure. We also describe proinflammatory cytokines as inductors of arrhythmia. We discuss ionic current alternation as possible mechanisms of cytokines action in heart. We consider TNF-α as a possible player in this signaling cascade. It was shown that TNF-α induced alternation of transmembrane action potentials. Influence of TNF-α on transient outward current (I to ), I Kur , I Kr , I Ks , I K1 is also reported. We discuss the interplay between TNF-α and Ca 2+ current, influence of TNF-α on SERCA. Then we consider influence of IL-1 on action potentials, I Na , I Ca , I K . We also address the role of IL-2, IL-6, and IL-11. Finally using TNF-α and IL-6 as an example we discuss the effects of cytokines on mechanoelectrical feedback. Perfusion of cardiac tissue with TNF-α containing solution leads to abnormalities in cardiac electrical activity, majorly to prolongation of APD90 and appearance of hump-like depolarization at APD90 level. After reaching E c hump-like depolarization transforms into extra-AP, leading to sustained arrhythmias. TNF-α activates NO cardiomyocyte synthases and the rise of intracellular NO levels opens MGCs, which leads to sodium entry into the cell, which depolarizes cellular membrane, shifting resting potential towards E C . We proposed and proved that TNF-α triggered arrhythmias can be mediated through activation of MGCs. Stretching of preparations removed TNF-α. Perfusion of preparation with IL-6 containing solution leads to fibrillation in response to low levels of stretch. IL-6 mechanisms of action are mediated by NO synthases A. Kamkin (B)

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Section: Cytokines and Mechanosensitivity Of The Heartmentioning

confidence: 57%

Section: Cytokines and Mechanosensitivity Of The Heartmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Proinflammatory Cytokines in Regulation of Cardiac Bioelectrical Activity: Link to Mechanoelectrical Feedback

Kuzmin¹,

Abramochkin²,

Mitrochin³

et al. 2011

Mechanical Stretch and Cytokines

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“…The effects of NO on myocardial functions including its pronounced influence on myocardium contraction and heart rhythm are described in another study (Kazanski et al, 2011). Moreover, a number of experiments conducted on whole hearts allows to suggest that NO and NO-synthases directly regulate the conductivity of mechanically gated channels (Kazanski et al, 2010a, b).…”

Section: Cell Signaling Of Interleukin-13 and Possible Mechanism Of Hmentioning

confidence: 97%

An Anti-inflammatory Cytokine Interleukin-13: Physiological Role in the Heart and Mechanoelectrical Feedback

Abramochkin

Makarenko

Mitrochin

et al. 2011

Mechanical Stretch and Cytokines

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The role of cytokines in responses not associated with inflammation as well as their involvement in regulation of non-haematopoietic cell activity is intensively studied during last decades. Control of heart activity can be carried out by pro-inflammatory cytokines. During the last decades considerable attention was drawn to the role of cytokines in physiological reactions not related to inflammation as well as their involvement in regulation of non-haematopoietic cell activity. An involvement of pro-inflammatory cytokines in the control of heart activity is thoroughly discussed in many publications. On the other hand such experimental data for the anti-inflammatory cytokines are currently absent. This review briefly summarizes existing evidences of involvement of anti-inflammatory cytokine interleukin-13 in the control of heart functioning and presents our latest findings on IL-13 influence on cardiomyocytes activity. According to our data, application of the IL-13 led to moderate acute changes in electrical activity of cardiomyocytes. At the same time it did not cause any electrical abnormalities, which is opposite to inflammatory cytokines application effects. Application of IL-13 reduced the effect of the mechanical stretch application on electrical activity of cardiomyocytes. Negative inotropic effect of anti-inflammatory IL-13 contrasts with positive inotropic effect of most pro-inflammatory cytokines. Special attention is given to possible mechanisms of IL-13-signaling and its influence on cardiac function in norm and pathology.

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“…The fact that, the negative ionotropic effect of IL-6 is mediated through myocardial NOS, from one and direct regulatory activity of NO on mechanically gated channels (MGCs) (Kazanski et al, 2011), from the other side, foster us to hypothesize the possible direct IL-6 induced MGCs alteration http://dx.doi.org/10.1016/j.imbio.2015.05.003 0171-2985/© 2015 Elsevier GmbH. All rights reserved.…”

Section: Introductionmentioning

confidence: 99%

Effects of interleukin-6 on the bio-electric activity of rat atrial tissue under normal conditions and during gradual stretching

Mitrokhin

Kamkin

2015

Immunobiology

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The Role of Nitric Oxide in the Regulation of Mechanically Gated Channels in the Heart

Cited by 7 publications

References 78 publications

The Role of Proinflammatory Cytokines in Regulation of Cardiac Bioelectrical Activity: Link to Mechanoelectrical Feedback

The Role of Proinflammatory Cytokines in Regulation of Cardiac Bioelectrical Activity: Link to Mechanoelectrical Feedback

An Anti-inflammatory Cytokine Interleukin-13: Physiological Role in the Heart and Mechanoelectrical Feedback

Effects of interleukin-6 on the bio-electric activity of rat atrial tissue under normal conditions and during gradual stretching

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