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

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Abstract
1 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. 2 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). 3 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. 4 Although threshold and latency of the e.j.p. were not affected by CTX-1 (≤400 pM), propagated impulses were blocked at ≥ 100 pM. 5 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) 6 All effects of CTX-1 were abolished by tetrodotoxin (0.3 μm). 7 Raised Ca2+ (6 mM) reduced the depolarization and spontaneous activity produced by CTX-1. 8 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). 9 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.