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Calcium channels involved in noradrenaline release from sympathetic neurones in rabbit carotid artery

Torben R Uhrenholt1, Ove A Nedergaard

  • 1Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark.

Pharmacology & Toxicology
|May 20, 2003
PubMed

Insights

N-type calcium channels mediate noradrenaline release from sympathetic nerves in rabbit carotid arteries. L-type calcium channels do not play a role, even when potassium channels are blocked, indicating specific channel involvement in neurotransmitter release.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cardiovascular Physiology

Background:

  • Transmitter release from nerve terminals relies on calcium ion (Ca2+) influx via voltage-gated calcium channels.
  • Sympathetic neurons possess both N-type and L-type calcium channels.
  • Potassium channel blockade can augment Ca2+ entry into sympathetic neurons.

Purpose of the Study:

  • To investigate the involvement of N-type and L-type calcium channels in the release of noradrenaline from vascular sympathetic neurons.
  • To determine if L-type calcium channels contribute to noradrenaline release, particularly under conditions of potassium channel blockade.

Main Methods:

  • Rabbit carotid artery rings were pre-incubated with [3H]-noradrenaline.
  • Electrical field stimulation was employed to induce 3H overflow, measuring noradrenaline release.
  • Selective N-type (omega-conotoxin GVIA) and L-type (nifedipine, nimodipine) calcium channel blockers were used, alongside a calcium channel opener (Bay K 8644) and a potassium channel blocker (4-aminopyridine).

Main Results:

  • Selective blockade of N-type calcium channels with omega-conotoxin GVIA dose-dependently reduced stimulation-evoked 3H overflow, with significant inhibition (91% Emax) at 3 x 10(-8) M.
  • Selective L-type calcium channel blockers (nifedipine, nimodipine) did not affect basal or stimulated 3H overflow.
  • Potassium channel blockade by 4-aminopyridine enhanced 3H overflow, but did not alter the inhibitory effect of omega-conotoxin GVIA, nor did L-type channel blockers show an effect in its presence.

Conclusions:

  • Stimulation-evoked noradrenaline release from sympathetic neurons in the rabbit carotid artery is primarily mediated by N-type calcium channels.
  • L-type calcium channels are not significantly involved in this process, even when neuronal excitability is increased by potassium channel blockade.

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