Premium
[Ca 2+ ] changes in sympathetic varicosities and Schwann cells in rat mesenteric arteries—Relation to noradrenaline release and contraction
Author(s) -
Hansen Thomas,
Tarasova Olga S.,
Khammy Makhala M.,
Ferreira Avelino,
Kennard James A.,
Andresen Jørgen,
Staehr Christian,
Brain Keith L.,
Nilsson Holger,
Aalkjær Christian
Publication year - 2019
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.13279
Subject(s) - chemistry , mesenteric arteries , voltage dependent calcium channel , acetylcholine , medicine , endocrinology , calcium , anatomy , biophysics , artery , biology
Aim This study aimed to assess intracellular Ca 2+ 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 Ca 2+ in nerves was assessed with confocal imaging, noradrenaline release with amperometry and artery tone with wire myography. Ca 2+ 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 Ca 2+ increase to ATP. Electrical field stimulation of nerves caused a frequency‐dependent increase in varicose [Ca 2+ ] ([Ca 2+ ] v ). ω‐conotoxin‐GVIA (100 nmol/L) reduced the [Ca 2+ ] 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 K V channel blocker, 4‐aminopyridine (10 µmol/L), increased [Ca 2+ ] v , noradrenaline release and force development both in the absence and presence of ω‐conotoxin‐GVIA. Yohimbine (1 µmol/L) increased both [Ca 2+ ] v and noradrenaline release but reduced force development. Acetylcholine (10 µmol/L) caused atropine‐sensitive inhibition of [Ca 2+ ] v , noradrenaline release and force. In the presence of ω‐conotoxin‐GVIA, acetylcholine caused a further inhibition of all parameters. Conclusion Modification of [Ca 2+ ] in arterial sympathetic axons and Schwann cells was assessed separately. K V 3.1 channels may be important regulators of [Ca 2+ ] v , noradrenaline release and force development. Presynaptic adrenoceptor and muscarinic receptor activation modify transmitter release through modification of [Ca 2+ ] v .