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[Ca2+ ] changes in sympathetic varicosities and Schwann cells in rat mesenteric arteries – relation to noradrenaline release and contractionстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 14 августа 2019 г.
- Авторы: Hansen T., Tarasova OS, Khammy MM, Ferreira A., Kennard JA, Andresen J., Staehr C., Brain KL, Nilsson H., Aalkjaer C.
- Журнал: Acta Physiologica
- Год издания: 2019
- Издательство: Blackwell Publishing Inc.
- Местоположение издательства: United Kingdom
- Первая страница: e13279
- DOI: 10.1111/apha.13279
- Аннотация: AIM: This study aimed to assess intracellular Ca2+ dynamics in nerve cells and Schwann cells in isolated rat resistance arteries and determine how these dynamics modify noradrenaline release from the nerves and consequent force development. METHODS: Ca2+ in nerves was assessed with confocal imaging, noradrenaline release with amperometry, and artery tone with wire myography. Ca2+ in axons was assessed after loading with Oregon Green 488 BAPTA-1 dextran. In other experiments, arteries were incubated with Calcium Green-1-AM which loads both axons and Schwann cells. RESULTS: Schwann cells but not axons responded with a Ca2+ increase to ATP. Electrical field stimulation of nerves caused a frequency dependent increase of varicose [Ca2+ ] ([Ca2+ ]v ). ω-conotoxin-GVIA (100 nM) reduced the [Ca2+ ]v transient to 2 Hz and 16 Hz by 60% and 27%, respectively; in contrast ω-conotoxin GVIA inhibited more than 80% of the noradrenaline release and force development at 2 and 16 Hz. The KV channel blocker, 4-aminopyridine (10 μM), increased [Ca2+ ]v , noradrenaline release, and force development both in the absence and presence of ω-conotoxin-GVIA. Yohimbine (1 μM) increased both [Ca2+ ]v and noradrenaline release but reduced force development. Acetylcholine (10 μM) caused atropine-sensitive inhibition of [Ca2+ ]v , noradrenaline release and force. In the presence of ω-conotoxin-GVIA, acetylcholine caused a further inhibition of all parameters. CONCLUSION:Modification of [Ca2+ ] in arterial sympathetic axons and Schwann cells was assessed separately. KV 3.1 channels may be important regulators of [Ca2+ ]v , noradrenaline release, and force development. Presynaptic adrenoceptor and muscarinic receptor activation modify transmitter release through modification of [Ca2+ ]v . This article is protected by copyright. All rights reserved.
- Добавил в систему: Тарасова Ольга Сергеевна