| Форма представления | Статьи в зарубежных журналах и сборниках |
| Год публикации | 2015 |
| Язык | английский |
|
Ситдикова Гузель Фаритовна, автор
|
|
Denis V. Abramochkin Olga P. Konovalova Andre Kamkin, автор
|
| Библиографическое описание на языке оригинала |
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 |
| Аннотация |
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 |
| Ключевые слова |
Carbon monoxide . Heart . Action potential .
Guanylate cyclase . cGMP. cAMP |
| Название журнала |
Journal of Physiology and
Biochemistry
|
| URL |
http://link.springer.com/article/10.1007%2Fs13105-015-0387-y |
| Пожалуйста, используйте этот идентификатор, чтобы цитировать или ссылаться на эту карточку |
https://repository.kpfu.ru/?p_id=112258 |
| Файлы ресурса | |
|
|
Полная запись метаданных  |
| Поле DC |
Значение |
Язык |
| dc.contributor.author |
Ситдикова Гузель Фаритовна |
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/?p_id=112258 |
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 |
Статьи в зарубежных журналах и сборниках |
ru_RU |
|
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