Effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline release and purinergic neuroeffector transmission in rat tail artery

The effects of Ca2+ concentration and Ca2+ 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 m...

Full description

Saved in:
Bibliographic Details
Published in:British journal of pharmacology 1999-01, Vol.126 (1), p.11-18
Main Authors: Brock, James A, Cunnane, Thomas C
Format: Article
Language:English
Subjects:
adenosine 5′‐triphosphate
Adenosine Triphosphate - metabolism
amperometry
Animals
Arteries - drug effects
Arteries - innervation
Arteries - metabolism
Biological and medical sciences
Ca2+ channel blockers
Ca2+ channels
Calcium - metabolism
Calcium - pharmacology
Calcium Channel Blockers - pharmacology
Dose-Response Relationship, Drug
Electrophysiology
Evoked Potentials - drug effects
Female
Fundamental and applied biological sciences. Psychology
In Vitro Techniques
Membrane Potentials - drug effects
neurotransmitter release
Nifedipine - pharmacology
noradrenaline
Norepinephrine - metabolism
omega-Conotoxin GVIA
omega-Conotoxins
Peptides - pharmacology
Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ
Postganglionic sympathetic nerve
rat tail artery
Rats
Rats, Wistar
Sympathetic Nervous System - drug effects
Sympathetic Nervous System - metabolism
Synaptic Transmission - drug effects
Tail
Vertebrates: nervous system and sense organs
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The effects of Ca2+ concentration and Ca2+ 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 Ca2+ 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 Ca2+ blocker, ω‐conotoxin GVIA (ω‐CTX GVIA, 0.1 μM) 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 Ca2+ channel blocker, Cd2+ (0.1 mM), and were reduced by ω‐conotoxin MVIIC (0.5 μM) and ω‐agatoxin IVA (40 nM). Nifedipine (10 μM) had no inhibitory effect on ω‐CTX GVIA resistant e.j.ps and NA‐induced oxidation currents. Thus both varying Ca2+ concentration and applying Ca2+ 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
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0702256