Electrical activity in rat tail artery during asynchronous activation of postganglionic nerve terminals by ciguatoxin‐1

Abstract

The effects of ciguatoxin‐1 (CTX‐1) on the membrane potential of smooth muscle cells have been examined in rat proximal tail arteries isolated in vitro. CTX‐1 (≥ 10 pM) increased the frequency of spontaneous excitatory junction potentials (s.ej.ps). At 100–400 pM, there was also a marked and maintained depolarization (19.7 ± 1.4 mV, n=14, at 400 pM). In 20–400 pM CTX‐1, perivascular stimuli evoked excitatory junction potentials (s.e.j.ps) which were prolonged in time course relative to control. Although threshold and latency of the e.j.p. were not affected by CTX‐1 (≤400 pM), propagated impulses were blocked at ≥ 100 pM. The spontaneous activity and the depolarization produced by CTX‐1 were reduced in the presence of Ca2+ (0.1 mM)/Mg2+ (25 mM), ω‐conotoxin (0.1 μm) or Cd2+ (50–100 μm) All effects of CTX‐1 were abolished by tetrodotoxin (0.3 μm). Raised Ca2+ (6 mM) reduced the depolarization and spontaneous activity produced by CTX‐1. In 400 pM CTX‐1, the membrane repolarized (17 ± 3.2 mV, n=4) following the addition of phentolamine (1 μm). S.e.j.ps and e.j.ps were selectively abolished by suramin (1 mM), and the membrane repolarized by 1.3±1.6 mV (n=4). We conclude that CTX‐1 releases noradrenaline and ATP by initiating asynchronous discharge of postganglionic perivascular axons. In 100–400 pM CTX‐1, the smooth muscle was depolarized to levels resembling those recorded in this artery during ongoing vasoconstrictor discharge in vivo. 1995 British Pharmacological Society