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- Title
L-type calcium channels in sympathetic α3 β2-n ACh R-mediated cerebral nitrergic neurogenic vasodilation.
- Authors
Wu, C. Y.‐C.; Lee, R. H.‐C.; Chen, P.‐Y.; Tsai, A. P.‐Y.; Chen, M.‐F.; Kuo, J.‐S.; Lee, T. J.‐F.
- Abstract
Aim Nicotine stimulation of α3 β2-nicotinic acetylcholine receptors ( α3 β2-n AChRs) located on sympathetic nerves innervating basilar arteries causes calcium-dependent noradrenaline release, leading to activation of parasympathetic nitrergic nerves and dilation of basilar arteries. This study aimed to investigate the major subtype of calcium channels located on cerebral peri-vascular sympathetic nerves, which is involved in nicotine-induced α3 β2-n AChR-mediated nitrergic vasodilation in basilar arteries. Methods Nicotine- and transmural nerve stimulation ( TNS)-induced dilation of isolated porcine basilar arteries was examined using in vitro tissue bath. Nicotine-induced calcium influx, nicotine-induced noradrenaline release and nicotine-induced inward currents were evaluated in rat superior cervical ganglion ( SCG) neurones, peri-vascular sympathetic nerves of porcine basilar arteries and α3 β2-n ACh Rs-expressing oocytes respectively. m RNA and protein expression of Cav1.2 and Cav1.3 channels were detected by RT- PCR, Western blotting and immunohistochemistry. Results Nicotine-induced vasodilation was not affected by ω -agatoxin TK (selective P/Q-type calcium channel blocker) or ω-conotoxin GVIA (N-type calcium channel blocker). The vasodilation, however, was inhibited by nicardipine (L-type calcium channel blocker) in concentrations which did not affect TNS-induced vasodilation, suggesting the specific blockade. Nicardipine concentration-dependently inhibited nicotine-induced calcium influx in rat SCG neurones and reduced nicotine-induced noradrenaline release from peri-vascular sympathetic nerves of porcine basilar arteries. Nicardipine (10 μ m), which significantly blocked nicotine-induced vasorelaxation by 70%, did not appreciably affect nicotine-induced inward currents in α3 β2-n AChRs-expressing oocytes. Furthermore, the m RNAs and proteins of Cav1.2 and Cav1.3 channels were expressed in porcine SCG and peri-vascular nerve terminals. Conclusion The sympathetic neuronal calcium influx through L-type calcium channels is modulated by α3 β2-n AChRs. This calcium influx causes noradrenaline release, initiating sympathetic-parasympathetic (axo-axonal) interaction-induced nitrergic dilation of porcine basilar arteries.
- Subjects
CALCIUM channels; NICOTINIC acetylcholine receptors; VASODILATION; NORADRENALINE regulation; NORADRENALINE; PROTEIN expression
- Publication
Acta Physiologica, 2014, Vol 211, Issue 4, p544
- ISSN
1748-1708
- Publication type
Article
- DOI
10.1111/apha.12315