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[Ca2+ ] changes in sympathetic varicosities and Schwann cells in rat mesenteric arteries-Relation to noradrenaline release and contraction.

Journal article
Authors Thomas Hansen
Olga S Tarasova
Makhala M Khammy
Avelino Ferreira
James A Kennard
Jørgen Andresen
Christian Staehr
Keith L Brain
Holger Nilsson
Christian Aalkjaer
Published in Acta physiologica (Oxford, England)
Volume 226
Issue 4
Pages e13279
ISSN 1748-1716
Publication year 2019
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages e13279
Language en
Links dx.doi.org/10.1111/apha.13279
www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords neurotransmission prejunctional modulation small arteries sympathetic nerve noradrenaline ATP
Subject categories Physiology

Abstract

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.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.Schwann cells but not axons responded with a Ca2+ increase to ATP. Electrical field stimulation of nerves caused a frequency-dependent increase in varicose [Ca2+ ] ([Ca2+ ]v ). ω-conotoxin-GVIA (100 nmol/L) reduced the [Ca2+ ]v transient to 2 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 µmol/L), increased [Ca2+ ]v , noradrenaline release and force development both in the absence and presence of ω-conotoxin-GVIA. Yohimbine (1 µmol/L) increased both [Ca2+ ]v and noradrenaline release but reduced force development. Acetylcholine (10 µmol/L) 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.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 .

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