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Effects of Ca 2+ concentration and Ca 2+ channel blockers on noradrenaline release and purinergic neuroeffector transmission in rat tail artery
Author(s) -
Brock James A,
Cunnane Thomas C
Publication year - 1999
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702256
Subject(s) - channel blocker , neurotransmission , excitatory postsynaptic potential , chemistry , biophysics , nifedipine , extracellular , calcium , biochemistry , biology , receptor , organic chemistry
The effects of Ca 2+ concentration and Ca 2+ channel blockers on noradrenaline (NA) and adenosine 5′‐triphosphate (ATP) release from postganglionic sympathetic nerves have been investigated in rat tail arteries in vitro . Intracellularly recorded excitatory junction potentials (e.j.ps) were used as a measure of ATP release and continuous amperometry was used to measure NA release. Varying the extracellular Ca 2+ concentration similarly affected the amplitudes of e.j.ps and NA‐induced oxidation currents evoked by trains of ten stimuli at 1 Hz. The N‐type Ca 2+ blocker, ω‐conotoxin GVIA (ω‐CTX GVIA, 0.1 μ M ) reduced the amplitudes of both e.j.ps (evoked by trains of ten stimuli at 1 Hz) and NA‐induced oxidation currents (evoked by trains of ten stimuli at 1 Hz and 50 stimuli at 10 Hz) by about 90%. The ω‐CTX GVIA resistant e.j.ps and NA‐induced oxidation currents evoked by trains of 50 stimuli at 10 Hz were abolished by the non‐selective Ca 2+ channel blocker, Cd 2+ (0.1 m M ), and were reduced by ω‐conotoxin MVIIC (0.5 μ M ) and ω‐agatoxin IVA (40 n M ). Nifedipine (10 μ M ) had no inhibitory effect on ω‐CTX GVIA resistant e.j.ps and NA‐induced oxidation currents. Thus both varying Ca 2+ concentration and applying Ca 2+ channel blockers results in similar effects on NA and ATP release from postganglionic sympathetic nerves. These findings are consistent with the hypothesis that NA and ATP are co‐released together from the sympathetic nerve terminals.British Journal of Pharmacology (1999) 126 , 11–18; doi: 10.1038/sj.bjp.0702256