Форма представления | Статьи в зарубежных журналах и сборниках |
Год публикации | 2015 |
Язык | английский |
|
Гиззатуллин Алмаз Рафаилович, автор
Лифанова Анастасия Сергеевна, автор
Ситдикова Гузель Фаритовна, автор
Хаертдинов Наиль Назимович, автор
|
Библиографическое описание на языке оригинала |
Khaertdinov N.N. Role of K(ATP)-channels in the effects of hydrogen sulfide on the contractility of rat ventricular myocardium/N.N. Khaertdinov, A.S. Lifanova, A.R. Gizzatullin, G.F. Sitdikova, //Genes and Cells. - 2015. - Vol.10, Is.4. - P.103-105. |
Аннотация |
The effect of sodium hydrosulfide (NaHS) - donor of hydrogen sulfide (H2S) on the force of contraction of isolated rat ventricle was studied. Application of NaHS in concentrations 1 and 10 μM resulted in an increase and in concentrations 50, 100, 200 and 300 μM - dosedependent decrease of the force of contraction. Inhibition of K-channels by tetraethylammonium (15 mM) caused the increase of the amplitude of contraction and the negative inotropic effect of NaHS (200 μM) was preserved. After the activation or inhibition of ATP-dependent K-channels by diazoxide (20 μM) or glibenclamide (50 μM), respectively, the negative inotropic effect of NaHS was the same as in control. After preliminary application of NaHS glibenclamide (50 μM) reversed the contraction force to yhe control values. The obtained data suppose that in the isolated rat ventricle exogenous H2S causes a reduction of the force of contraction, which is mediated by the activation of ATPdependent K-channels. |
Ключевые слова |
hydrogen sulfide, contraction, K(ATP)-channels |
Название журнала |
Genes and Cells
|
URL |
http://www.scopus.com/inward/record.url?eid=2-s2.0-84962213101&partnerID=40&md5=714bc5726d87f404e332d10597d73bd0 |
Пожалуйста, используйте этот идентификатор, чтобы цитировать или ссылаться на эту карточку |
https://repository.kpfu.ru/?p_id=130569 |
Полная запись метаданных |
Поле DC |
Значение |
Язык |
dc.contributor.author |
Гиззатуллин Алмаз Рафаилович |
ru_RU |
dc.contributor.author |
Лифанова Анастасия Сергеевна |
ru_RU |
dc.contributor.author |
Ситдикова Гузель Фаритовна |
ru_RU |
dc.contributor.author |
Хаертдинов Наиль Назимович |
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 |
Khaertdinov N.N. Role of K(ATP)-channels in the effects of hydrogen sulfide on the contractility of rat ventricular myocardium/N.N. Khaertdinov, A.S. Lifanova, A.R. Gizzatullin, G.F. Sitdikova, //Genes and Cells. - 2015. - Vol.10, Is.4. - P.103-105. |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/?p_id=130569 |
ru_RU |
dc.description.abstract |
Genes and Cells |
ru_RU |
dc.description.abstract |
The effect of sodium hydrosulfide (NaHS) - donor of hydrogen sulfide (H2S) on the force of contraction of isolated rat ventricle was studied. Application of NaHS in concentrations 1 and 10 μM resulted in an increase and in concentrations 50, 100, 200 and 300 μM - dosedependent decrease of the force of contraction. Inhibition of K-channels by tetraethylammonium (15 mM) caused the increase of the amplitude of contraction and the negative inotropic effect of NaHS (200 μM) was preserved. After the activation or inhibition of ATP-dependent K-channels by diazoxide (20 μM) or glibenclamide (50 μM), respectively, the negative inotropic effect of NaHS was the same as in control. After preliminary application of NaHS glibenclamide (50 μM) reversed the contraction force to yhe control values. The obtained data suppose that in the isolated rat ventricle exogenous H2S causes a reduction of the force of contraction, which is mediated by the activation of ATPdependent K-channels. |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
hydrogen sulfide |
ru_RU |
dc.subject |
contraction |
ru_RU |
dc.subject |
K(ATP)-channels |
ru_RU |
dc.title |
Role of K(ATP)-channels in the effects of hydrogen sulfide on the contractility of rat ventricular myocardium |
ru_RU |
dc.type |
Статьи в зарубежных журналах и сборниках |
ru_RU |
|