Transmitter release from nerve terminals is dependent on the entry of Ca(2+) 
through neuronal voltage-gated calcium channels. In sympathetic neurones both N- 
and L-type calcium channels are present. Potassium channel blockade increases 
Ca(2+) entry into sympathetic neurones. We examined the participation of N- and 
L-type calcium channels in the stimulation-evoked release of noradrenaline from 
vascular sympathetic neurones. Rings of rabbit carotid artery were preincubated 
with [3H]-noradrenaline. Electrical field stimulation was used to evoke 3H 
overflow. The selective N-type calcium channel blocking agent omega-conotoxin 
GVIA (single concentrations: 3 x 10(-10)-10(-8) M) caused a slowly developing 
reduction of the stimulation-evoked 3H overflow. At 3 x 10(-8) M, 
omega-conotoxin GVIA caused an equilibrium block with a rapid (15 min.) onset. 
After 2 hr exposure to omega-conotoxin the inhibition was steady (pIC50 (-log 
M): 9.43; Emax: 91%). The selective L-type calcium blocking agents nifedipine 
(10(-7)-10(-5) M) and nimodipine (10(-8)-10(-5) M) had no effect on the 
stimulation-evoked 3H overflow. The calcium channel opener Bay K 8644 (10-6 M) 
likewise had no effect. The potassium channel blocking agent 4-aminopyridine 
(10-5-10-3 M) enhanced the stimulation-evoked 3H overflow up to 5 times. 
4-Aminopyridine (10(-4) M) did not alter the inhibitory effect of 
omega-conotoxin GVIA (3 x 10(-8) M). In the presence of 4-aminopyridine (10(-4) 
M), nifedipine (10(-5) M) and nimodipine (10(-6) M) enhanced the 3H overflow. We 
conclude that the stimulation-evoked release of noradrenaline from sympathetic 
neurones in rabbit carotid artery is mediated by N-type calcium channels and 
that L-type channels are not involved even when potassium channels are blocked 
by 4-aminopyridine.