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Involvement of Different Calcium Channels in the Depolarization‐Evoked Release of Noradrenaline from Sympathetic Neurones in Rabbit Carotid Artery *
Author(s) -
Uhrenholt Torben R.,
Nedergaard Ove A.
Publication year - 2005
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2005.pto_90.x
Subject(s) - mibefradil , stimulation , voltage dependent calcium channel , nimodipine , chemistry , calcium channel , medicine , calcium , channel blocker , nifedipine , depolarization , endocrinology
The calcium channels coupled to noradrenaline release from sympathetic neurones in the rabbit isolated carotid artery were examined. Rings of carotid artery were preloaded with (‐)‐[ 3 H]noradrenaline and the fractional 3 H overflow evoked by electrical‐field stimulation was determined by liquid scintillation spectrometry. The N‐type Ca 2+ channel blocking agent ω‐conotoxin GVIA (3×10 −9 ‐6×10 −8 M) reduced the stimulation‐evoked 3 H overflow. The maximal inhibition was seen with 3×10 −8 M. The maximal reduction was more marked at a low (2 Hz) stimulation frequency than at a high one (30 Hz). Mibefradil (10 −6 M) irreversibly reduced the 3 H overflow evoked by field stimulation (2 Hz). At 30 Hz, the reduction was more marked than at 2 Hz. Mibefradil (3×10 −6 –10 −5 M) enhanced the passive 3 H outflow. The reduction of the stimulation (30 Hz)‐evoked 3 H overflow seen with ω‐conotoxin GVIA (3×10 −8 M) was enhanced by mibefradil (10 −6 M) and unaffected by nimodipine (10 −5 M) and ω‐agatoxin IVA (10 −8 M). We conclude that the stimulation‐evoked release of noradrenaline from sympathetic neurones in rabbit carotid artery at a low frequency (2 Hz) is mediated mainly by the N‐type calcium channels. At a high frequency (30 Hz), T‐type Ca 2+ channels are also involved.