Evidence map›Paper›PMID 20157389›Full record

ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2008

Roles of dopaminergic d(1) and d(2) receptors in catecholamine release from the rat adrenal medulla.

Young Joo Baek, Yoo Seong Seo, Dong Yoon Lim

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In one paragraph

Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Young Joo BaekDepartment of Pharmacology, College of Medicine, Chosun University, Gwangju 501-759, Korea.
Yoo Seong Seo
Dong Yoon Lim
Chosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was designed to establish comparatively the inhibitory effects of D(1)-like and D(2)-like dopaminergic receptor agonists, SKF81297 and R(-)-TNPA on the release of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. SKF81297 (30microM) and R-(-)-TNPA (30microM) perfused into an adrenal vein for 60 min, produced great inhibition in the CA secretory responses evoked by ACh (5.32x10(- 3) M), DMPP (10(-4) M), McN-A-343 (10(-4) M), high K(+) (5.6x10(-2) M), Bay-K-8644 (10microM), and cyclopiazonic acid (10microM), respectively. For the release of CA evoked by ACh, high K(+), DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid, the following rank order of inhibitory potency was obtained: SKF81297>R-(-)-TNPA. However, R(+)-SCH23390, a selectve D(1)-like dopaminergic receptor antagonist, and S(-)-raclopride, a selectve D(2)-like dopaminergic receptor antagonist, enhanced the CA secretory responses evoked by ACh, high K(+), DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid only for 0~4 min. The rank order for the enhancement of CA release evoked by high K(+), McN-A-343 and cyclopiazonic acid was R(+)-SCH23390>S(-)-raclopride. Also, the rank order for ACh, DMPP and Bay-K-8644 was S(-)-raclopride > R(+)-SCH23390. Taken together, these results demonstrate that both SKF81297 and R-(-)-TNPA inhibit the CA release evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization from the isolated perfused rat adrenal gland without affecting the basal release, respectively, but both R(+)-SCH23390 and S(-)-raclopride facilitate the CA release evoked by them. It seems likely that the inhibitory effects of SKF81297 and R-(-)-TNPA are mediated by the activation of D(1)-like and D(2)-like dopaminergic receptors located on the rat adrenomedullary chromaffin cells, respectively, whereas the facilitatory effects of R(+)-SCH23390 and S(-)-raclopride are mediated by the blockade of D(1)-like and D(2)-like dopaminergic receptors, respectively: this action is possibly associated with extra- and intracellular calcium mobilization. Based on these results, it is thought that the presence of dopaminergic D(1) receptors may play an important role in regulation of the rat adrenomedullary CA secretion, in addition to well-known dopaminergic D(2) receptors.

Indexed as

Adrenal meduulaCatecholamine secretionDopaminergic receptorsR(+)-SCH23390R-(-)TNPASKF81297S(-)-raclopride

Identifiers

PMID20157389
PMCPMC2817528
OpenAlexW2119567697

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.