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A Dihydropyridine‐Resistant Component in the Rat Adrenal Secretory Response to Splanchnic Nerve Stimulation
Author(s) -
López M. G.,
Shukla R.,
García A. G.,
Wakade A. R.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb10956.x
Subject(s) - endocrinology , splanchnic nerves , stimulation , medicine , adrenal medulla , isradipine , dihydropyridine , acetylcholine , nicotinic agonist , chemistry , splanchnic , muscarinic acetylcholine receptor , receptor , biology , catecholamine , calcium , blood flow
A study of the effects of dihydropyridine Ca 2+ channel modulators on the release of catecholamines from perfused rat adrenal glands, evoked by electrical stimulation of their splanchnic nerves, is presented. Electrically mediated secretory responses were compared to chemically mediated responses (exogenous acetylcholine, nicotine, or high K + ). Intensities of stimuli were selected to produce quantitatively similar secretory responses (between 100 and 200 ng per stimulus). The main finding of the study is that responses to transmural stimulation (300 pulses at 1 or 10 Hz) and to acetylcholine were inhibited only partially (about 50%) by isradipine, an L‐type Ca 2+ channel blocker. In contrast, responses to high K + (17.5 m M for 2 min) were highly sensitive to isradipine (IC 50 = 8.2 n M ). Responses to nicotine were also fully inhibited by this drug. Bay K 8644 (an L‐type Ca 2+ channel activator) potentiated mildly the secretory responses to electrical stimulation at 10 Hz and to acetylcholine, but increased threefold the responses to K + and nicotine. It is, therefore, likely that responses mediated by high K + or nicotinic receptors are triggered by external Ca 2+ gaining access to the internal secretory machinery through L‐type, dihydropyridine‐sensitive voltage‐dependent Ca 2+ channels. However, in addition to nicotinic receptors, the physiological stimulation of adrenal medulla chromaffin cells through splanchnic nerves has other components, i.e., muscarinic receptor stimulation or the release of cotransmitters such as vasoactive intestinal polypeptide. The poorer sensitivity to dihydropyridines of secretory responses triggered by electrical stimulation of splanchnic nerve terminals or exogenous acetylcholine speaks in favor of alternative Ca 2+ pathways, probably some dihydropyri‐dine‐resistant Ca 2+ channels, in modulating the physiological adrenal catecholamine secretory process.