Article date: March 2004
By: Judy L Morris, Daina I Ozols, Richard J Lewis, Ian L Gibbins, Phillip Jobling in Volume 141, Issue 6, pages 961-970
The effects of calcium channel blockers on co‐transmission from different populations of autonomic vasomotor neurons were studied on isolated segments of uterine artery and vena cava from guinea‐pigs.
Sympathetic, noradrenergic contractions of the uterine artery (produced by 200 pulses at 1 or 10 Hz; 600 pulses at 20 Hz) were abolished by the N‐type calcium channel blocker ω‐conotoxin (CTX) GVIA at 1–10 nM.
Biphasic sympathetic contractions of the vena cava (600 pulses at 20 Hz) mediated by noradrenaline and neuropeptide Y were abolished by 10 nM CTX GVIA.
Neurogenic relaxations of the uterine artery (200 pulses at 10 Hz) mediated by neuronal nitric oxide and neuropeptides were reduced <50% by CTX GVIA 10–100 nM.
Capsaicin (3 μM) did not affect the CTX GVIA‐sensitive or CTX GVIA‐resistant neurogenic relaxations of the uterine artery.
The novel N‐type blocker CTX CVID (100–300 nM), P/Q‐type blockers agatoxin IVA (10–100 nM) or CTX CVIB (100 nM), the L‐type blocker nifedipine (10 μM) or the ‘R‐type’ blocker SNX‐482 (100 nM), all failed to reduce CTX GVIA‐resistant relaxations. The T‐type channel blocker NiCl2 (100–300 μM) reduced but did not abolish the remaining neurogenic dilations.
Release of different neurotransmitters from the same autonomic vasomotor axon depends on similar subtypes of calcium channels. N‐type channels are responsible for transmitter release from vasoconstrictor neurons innervating a muscular artery and capacitance vein, but only partly mediate release of nitric oxide and neuropeptides from pelvic vasodilator neurons.
The effects of calcium channel blockers on co‐transmission from different populations of autonomic vasomotor neurons were studied on isolated segments of uterine artery and vena cava from guinea‐pigs.
Sympathetic, noradrenergic contractions of the uterine artery (produced by 200 pulses at 1 or 10 Hz; 600 pulses at 20 Hz) were abolished by the N‐type calcium channel blocker ω‐conotoxin (CTX) GVIA at 1–10 nM.
Biphasic sympathetic contractions of the vena cava (600 pulses at 20 Hz) mediated by noradrenaline and neuropeptide Y were abolished by 10 nM CTX GVIA.
Neurogenic relaxations of the uterine artery (200 pulses at 10 Hz) mediated by neuronal nitric oxide and neuropeptides were reduced <50% by CTX GVIA 10–100 nM.
Capsaicin (3 μM) did not affect the CTX GVIA‐sensitive or CTX GVIA‐resistant neurogenic relaxations of the uterine artery.
The novel N‐type blocker CTX CVID (100–300 nM), P/Q‐type blockers agatoxin IVA (10–100 nM) or CTX CVIB (100 nM), the L‐type blocker nifedipine (10 μM) or the ‘R‐type’ blocker SNX‐482 (100 nM), all failed to reduce CTX GVIA‐resistant relaxations. The T‐type channel blocker NiCl2 (100–300 μM) reduced but did not abolish the remaining neurogenic dilations.
Release of different neurotransmitters from the same autonomic vasomotor axon depends on similar subtypes of calcium channels. N‐type channels are responsible for transmitter release from vasoconstrictor neurons innervating a muscular artery and capacitance vein, but only partly mediate release of nitric oxide and neuropeptides from pelvic vasodilator neurons.
British Journal of Pharmacology (2004) 141, 961–970. doi:10.1038/sj.bjp.0705712
DOI: 10.1038/sj.bjp.0705712
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