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Calcium channel subtypes for the sympathetic and parasympathetic nerves of guinea‐pig atria
Author(s) -
Hong S.J.,
Chang C.C.
Publication year - 1995
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 - 10.1111/j.1476-5381.1995.tb16375.x
Subject(s) - chronotropic , medicine , carbachol , nifedipine , propranolol , channel blocker , endocrinology , stimulation , atropine , acetylcholine , inotrope , chemistry , calcium , heart rate , blood pressure
1 The Ca 2+ channel subtypes of the autonomic nerves of guinea‐pig atria were elucidated by monitoring the effects of specific Ca 2+ channel blockers on the negative and positive inotropic responses associated respectively, with stimulation of the parasympathetic and sympathetic nerves. 2 In left atria paced at 2–4 Hz, the negative inotropic effect induced by field stimulation of parasympathetic nerves (in the presence of propranolol) was abolished by ω‐conotoxin MVIIC, a blocker of N‐type and OPQ subfamily Ca 2+ channels. ω‐Conotoxin GVIA (an N‐type blocker), ω‐agatoxin IVA (a P‐type blocker), nifedipine (an L‐type blocker) and Ni 2+ (a T‐ and R‐type blocker) were much less effective. 3 The positive inotropic response resulting from field stimulation of the sympathetic nerves (in the presence of atropine) was abolished by both ω‐conotoxins, while ω‐agatoxin IVA, nifedipine and Ni 2+ were ineffective. 4 In the spontaneously beating right atria, the early negative inotropic effect produced by 1,1‐dimethyl‐4‐phenylpiperazinium was abolished by ω‐conotoxin MVIIC; whereas the late positive inotropic effect was partially reduced, but not abolished, by a high concentration of ω‐conotoxin GVIA. 5 None of the peptide toxins affected the chronotropic and the inotropic responses evoked by carbachol and isoprenaline. 6 These results suggested that, under physiological conditions, the release of acetylcholine from paraysmpathetic nerves is dominated by an OPQ subfamily Ca 2+ channel while that of noradrenaline from sympathetic nerves is controlled by an N‐type Ca 2+ channel. Ligand‐induced noradrenaline release appeared to recruit additional type(s) of Ca 2+ channel.