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Diadenosine polyphosphates alter heart bioelectrical activity in rodent and non-rodent via different receptors and signalling pathwaysстатья Тезисы
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 12 июля 2017 г.
- Авторы: Pustovit K.B., Kuzmin V.S., Abramochkin D.V.
- Журнал: Acta Physiologica
- Том: 219
- Год издания: 2016
- Издательство: Blackwell Publishing Inc.
- Местоположение издательства: United Kingdom
- Первая страница: 21
- Последняя страница: 21
- DOI: 10.1111/apha.12841
- Аннотация: Introduction Extracellular diadenosine polyphosphates are considered as novel regulatory compounds, which have been identified also in myocardium. Effects of diadenosine polyphosphates in heart were investigated poorly. The aim of the present study was to reveal mechanisms of diadenosine tetra- and pentaphosphate (Ap4A/Ap5A) action in rodent and non-rodent myocardium. Methods Multicellular preparations of atrial and ventricle myocardium of Wistar rats (male, 200–250 g) and guinea-pigs (male, 300–350 g, GP) were perfused with Tyrode solution. Action potentials (AP) were recorded with use of standard microelectrode technique, and alteration of AP duration was estimated in the presence of Ap4A, Ap5A alone or with P1, P2 purine receptors antagonists. Alterations of cardiac inward rectifier potassium (IKAch) and calcium (ICaL) currents were measured by using standard whole-cell voltage clamp technique in isolated rat and GP cardiomyocytes in response to application of Ap4A/Ap5A. Results Administration of Ap4A/Ap5A caused a significant decrease in AP duration in both rat and GP myocardium. P1 receptor antagonist DPCPX completely suppressed effects of Ap4A/Ap5A in GP. However, DPCPX suppressed less than half of diadenosine polyphosphates effect in rat. P2 receptors antagonists (suramine, PPADS) were ineffective in GP, but significantly suppressed Ap4A/Ap5A-induced AP shortening in rat. Ap4A/Ap5A significantly enhanced IKACh in GP, but in rat both compounds failed to alter IKACh, however suppressed ICaL. Conclusion Ap4A/Ap5A affects AP in rat and GP myocardium via different mechanisms. While effects of diadenosine polyphosphates in GP are mediated by P1/Gi/IKACh pathway, in rat heart Ap4A/Ap5A activates P1 and P2 receptors equally and involves P2/Gq11 pathways.
- Добавил в систему: Пустовит Оксана Борисовна