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

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