Form of presentation | Articles in international journals and collections |
Year of publication | 2015 |
Язык | английский |
|
Sitdikova Guzel Faritovna, author
|
|
Denis V. Abramochkin Olga P. Konovalova Andre Kamkin, author
|
Bibliographic description in the original language |
Abramochkin, D.V.,Konovalova, O.P., Kamkin, A.,Sitdikova, G.F. Carbon monoxide modulates electrical activity of murine myocardium via cGMP-dependent mechanisms Journal of Physiology and Biochemistry Volume 71, Issue 1, 2015, P.107-119 |
Annotation |
Carbon monoxide (CO) is critical in cell
signaling, and inhalation of gaseous CO can impact
cardiovascular physiology. We have investigated
electrophysiological effects of CO and their
potential cGMP-dependent mechanism in isolated
preparations of murine myocardium. The standard microelectrode
technique was used to record myocardial
action potentials (APs). Exogenous CO (0.96×10−4?
4.8×10−4 M) decreased AP duration in atrial and ventricular
tissue and accelerated pacemaking activity in
sinoatrial node. Inhibitors of heme oxygenases (zinc
and tin protoporphyrin IX), which are responsible for
endogenous CO production, induced the opposite effects.
Inhibitor of soluble guanylate cyclase (sGC),
ODQ (10−5 M) halved CO-induced AP shortening,
while sGC activator azosidnone (10−5 M-3×10−4 M)
and cGMP analog BrcGMP (3×10−
4 M) induced
the same effects as CO. To see if CO effects are
attributed to differential regulation of phosphodiesterase
2 (PDE2) and 3 (PDE3), we used inhibitors
of these enz |
Keywords |
Carbon monoxide . Heart . Action potential .
Guanylate cyclase . cGMP. cAMP |
The name of the journal |
Journal of Physiology and
Biochemistry
|
URL |
http://link.springer.com/article/10.1007%2Fs13105-015-0387-y |
Please use this ID to quote from or refer to the card |
https://repository.kpfu.ru/eng/?p_id=112258&p_lang=2 |
Resource files | |
|
Full metadata record ![](https://shelly.kpfu.ru/pdf/picture/arrow_black_right.gif) |
Field DC |
Value |
Language |
dc.contributor.author |
Sitdikova Guzel Faritovna |
ru_RU |
dc.contributor.author |
Denis V. Abramochkin Olga P. Konovalova Andre Kamkin |
ru_RU |
dc.date.accessioned |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2015 |
ru_RU |
dc.identifier.citation |
Abramochkin, D.V.,Konovalova, O.P., Kamkin, A.,Sitdikova, G.F. Carbon monoxide modulates electrical activity of murine myocardium via cGMP-dependent mechanisms Journal of Physiology and Biochemistry Volume 71, Issue 1, 2015, P.107-119 |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/eng/?p_id=112258&p_lang=2 |
ru_RU |
dc.description.abstract |
Journal of Physiology and
Biochemistry |
ru_RU |
dc.description.abstract |
Carbon monoxide (CO) is critical in cell
signaling, and inhalation of gaseous CO can impact
cardiovascular physiology. We have investigated
electrophysiological effects of CO and their
potential cGMP-dependent mechanism in isolated
preparations of murine myocardium. The standard microelectrode
technique was used to record myocardial
action potentials (APs). Exogenous CO (0.96×10−4?
4.8×10−4 M) decreased AP duration in atrial and ventricular
tissue and accelerated pacemaking activity in
sinoatrial node. Inhibitors of heme oxygenases (zinc
and tin protoporphyrin IX), which are responsible for
endogenous CO production, induced the opposite effects.
Inhibitor of soluble guanylate cyclase (sGC),
ODQ (10−5 M) halved CO-induced AP shortening,
while sGC activator azosidnone (10−5 M-3×10−4 M)
and cGMP analog BrcGMP (3×10−
4 M) induced
the same effects as CO. To see if CO effects are
attributed to differential regulation of phosphodiesterase
2 (PDE2) and 3 (PDE3), we used inhibitors
of these enz |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
|
ru_RU |
dc.title |
Carbon monoxide modulates electrical activity of murine myocardium via cGMP-dependent mechanisms |
ru_RU |
dc.type |
Articles in international journals and collections |
ru_RU |
|