Institut for Biomedicin

Christian Aalkjær

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

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DOI

AimThis 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.

MethodsCa(2+) 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.

ResultsSchwann 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)). omega-conotoxin-GVIA (100nmol/L) reduced the [Ca2+](v) transient to 2 and 16Hz by 60% and 27%, respectively; in contrast omega-conotoxin GVIA inhibited more than 80% of the noradrenaline release and force development at 2 and 16Hz. The K-V channel blocker, 4-aminopyridine (10 mu mol/L), increased [Ca2+](v), noradrenaline release and force development both in the absence and presence of omega-conotoxin-GVIA. Yohimbine (1 mu mol/L) increased both [Ca2+](v) and noradrenaline release but reduced force development. Acetylcholine (10 mu mol/L) caused atropine-sensitive inhibition of [Ca2+](v), noradrenaline release and force. In the presence of omega-conotoxin-GVIA, acetylcholine caused a further inhibition of all parameters.

ConclusionModification of [Ca2+] in arterial sympathetic axons and Schwann cells was assessed separately. K(V)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).

OriginalsprogEngelsk
Artikelnummere13279
TidsskriftActa Physiologica
Vol/bind226
Nummer4
Antal sider11
ISSN1748-1708
DOI
StatusUdgivet - aug. 2019

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