Studies on secretion of catecholamines evoked by acetylcholine or transmural stimulation of the rat adrenal gland.

Wakade, Arun R.

doi:10.1113/jphysiol.1981.sp013676

Cited by 159 publications

(127 citation statements)

References 34 publications

(34 reference statements)

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“…Since chromaffin cells are the main source of circulating epinephrine, it is of interest to investigate how they ensure increased secretion upon stressful situations. Catecholamine secretion is regulated by both synaptic release of acetylcholine from splanchnic nerve terminals synapsing onto chromaffin cells (Douglas, 1968;Wakade, 1981) and local gap junction-mediated communication between chromaffin cells (Martin et al, 2001;Colomer et al, 2009). It is noteworthy that the cholinergic synaptic activity exerts a tonic inhibitory control on gap junctional coupling (Martin et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Colomer

Olivos-Oré²,

Vincent³

et al. 2010

J. Neurosci.

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An increase in circulating adrenal catecholamine levels constitutes one of the mechanisms whereby organisms cope with stress. Accordingly, stimulus-secretion coupling within the stressed adrenal medullary tissue undergoes persistent remodeling. In particular, cholinergic synaptic neurotransmission between splanchnic nerve terminals and chromaffin cells is upregulated in stressed rats. Since synaptic transmission is mainly supported by activation of postsynaptic neuronal acetylcholine nicotinic receptors (nAChRs), we focused our study on the role of ␣9-containing nAChRs, which have been recently described in chromaffin cells. Taking advantage of their specific blockade by the ␣-conotoxin RgIA (␣-RgIA), we unveil novel functional roles for these receptors in the stimulus-secretion coupling of the medulla. First, we show that in rat acute adrenal slices, ␣9-containing nAChRs codistribute with synaptophysin and significantly contribute to EPSCs. Second, we show that these receptors are involved in the tonic inhibitory control exerted by cholinergic activity on gap junctional coupling between chromaffin cells, as evidenced by an increased Lucifer yellow diffusion within the medulla in ␣-RgIA-treated slices. Third, we unexpectedly found that ␣9-containing nAChRs dominantly (Ͼ70%) contribute to acetylcholine-induced current in cold-stressed rats, whereas ␣3 nAChRs are the main contributing channels in unstressed animals. Consistently, expression levels of ␣9 nAChR transcript and protein are overexpressed in cold-stressed rats. As a functional relevance, we propose that upregulation of ␣9-containing nAChR channels and ensuing dominant contribution in cholinergic signaling may be one of the mechanisms whereby adrenal medullary tissue appropriately adapts to increased splanchnic nerve electrical discharges occurring in stressful situations.

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Section: Introductionmentioning

confidence: 99%

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Colomer

Olivos-Oré²,

Vincent³

et al. 2010

J. Neurosci.

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“…The adrenal gland was isolated by the methods described previously (Wakade, 1981). The abdomen was opened by a midline incision, and the left adrenal gland and surrounding area were exposed by placing three hook retractors.…”

Section: Methodsmentioning

confidence: 99%

“…CA content of perfusate was measured directly using the fluorometric method of Anton and Sayre (1962) without the intermediate purification alumina for the reasons described earlier (Wakade, 1981) using fluorospectrophotometer (Kontron Co., Milano, Italy).…”

Section: Easurement Of Catecholaminesmentioning

confidence: 99%

Resveratrol Inhibits Nicotinic Stimulation-Evoked Catecholamine Release from the Adrenal Medulla

Woo

Lim

2008

Korean J Physiol Pharmacol

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Resveratrol has been known to possess various potent cardiovascular effects in animal, but there is little information on its functional effect on the secretion of catecholamines (CA) from the perfused model of the adrenal medulla. Therefore, the aim of the present study was to determine the effect of resveratrol on the CA secretion from the isolated perfused model of the normotensive rat adrenal gland, and to elucidate its mechanism of action. Resveratrol (

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Section: Methodsmentioning

confidence: 99%

Inhibitory Effects of Dihydrexidine on Catecholamine Release from the Rat Adrenal Medulla

Lee¹,

Lim²,

Lim³

2009

Biomolecules and Therapeutics

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-The purpose of the present study was to examine the effect of dihydrexidine, a full D 1 receptor agonist, on the secretion of catecholamines (CA) from the perfused model of the rat adrenal gland, and to establish its mechanism of action. Dihydrexidine (10-100 μM), perfused into an adrenal vein for 60 min, relatively produced dose-and time-dependent inhibition in the CA secretory responses evoked by ACh (5.32 mM), high K ＋ (56 mM), DMPP (100 μM) and McN-A-343 (100 μM). Dihydrexidine itself did fail to affect basal CA output. Also, in adrenal glands loaded with dihydrexidine (30 μM), the CA secretory responses evoked by Bay-K-8644 (10 μM), an activator of L-type Ca 2＋ channels, cyclopiazonic acid (10 μM), an inhibitor of cytoplasmic Ca 2＋ -ATPase, and veratridine, an activator of voltage-dependent Na ＋ channels (10 μM), were also markedly inhibited, respectively. However, in the simultaneous presence of dihydrexidine (30 μM) and R (＋)-SCH23390 (a selective antagonist of D 1 receptor, 3 μM), the CA secretory responses evoked by ACh, high K ＋ , DMPP, McN-A-343, Bay-K-8644, cyclopiazonic acid and veratridine were considerably recovered to the extent of the corresponding control secretion compared with the inhibitory responses by dihydrexidinetreatment alone. In conclusion, these experimental results suggest that dihydrexidine significantly inhibits the CA secretion evoked by cholinergic stimulation (both nicotinic and muscarinic receptors) and membrane depolarization from the rat adrenal medulla. It seems that this inhibitory effect of dihydrexidine may be mediated by inhibiting influx of both Ca 2＋ and Na ＋ into the cytoplasm as well as by suppression of Ca 2＋ release from cytoplasmic calcium store through activation of dopaminergic D1 receptors located on the rat adrenomedullary chromaffin cells.

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Studies on secretion of catecholamines evoked by acetylcholine or transmural stimulation of the rat adrenal gland.

Cited by 159 publications

References 34 publications

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Resveratrol Inhibits Nicotinic Stimulation-Evoked Catecholamine Release from the Adrenal Medulla

Inhibitory Effects of Dihydrexidine on Catecholamine Release from the Rat Adrenal Medulla

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