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Titolo:
Glucocorticoid treatment increases inhibitory M-2 muscarinic receptor expression and function in the airways
Autore:
Jacoby, DB; Yost, BL; Kumaravel, B; Yee, CL; Xiao, HQ; Kawashima, K; Fryer, AD;
Indirizzi:
Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD USA Johns Hopkins Univ Baltimore MD USA m & Crit Care Med, Baltimore, MD USA Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA Johns Hopkins Univ Baltimore MD USA Environm Hlth Sci, Baltimore, MD USA Kyoritsu Coll Pharm, Dept Pharmacol, Tokyo, Japan Kyoritsu Coll Pharm Tokyo Japan oll Pharm, Dept Pharmacol, Tokyo, Japan
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 4, volume: 24, anno: 2001,
pagine: 485 - 491
SICI:
1044-1549(200104)24:4<485:GTIIMM>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
PULMONARY PARASYMPATHETIC NERVES; GUINEA-PIG; RAT-BRAIN; DEXAMETHASONE; ASTHMA; BRONCHOCONSTRICTION; CORTICOSTEROIDS; MODULATION; HISTAMINE; PROTEIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Jacoby, DB Johns Hopkins Sch Publ Hlth, 615 N Wolfe St, Baltimore, MD 21205 USA Johns Hopkins Sch Publ Hlth 615 N Wolfe St Baltimore MD USA 21205
Citazione:
D.B. Jacoby et al., "Glucocorticoid treatment increases inhibitory M-2 muscarinic receptor expression and function in the airways", AM J RESP C, 24(4), 2001, pp. 485-491

Abstract

M-2 muscarinic receptors on parasympathetic nerve endings inhibit acetylcholine release in the airways. In this study, the effects of dexamethasone on M-2 receptors in vivo and in primary cultures of airway parasympathetic neurons were tested. Treating guinea pigs with dexamethasone (0.1 mg/kg, daily for 2 d) substantially increased inhibitory M-2 muscarinic receptor function, decreasing airway responsiveness to electrical stimulation of the vagi, At the same time, dexamethasone decreased the response to acetylcholine but not to methacholine, suggesting that cholinesterase activity was increased. When both cholinesterase and M-2 receptors were blocked (using physostigmine and gallamine, respectively) vagally induced bronchoconstriction wasincreased to control values. In primary cultures of airway parasympatheticneurons, dexamethasone significantly decreased the release of acetylcholine in response to electrical stimulation. Blocking inhibitory M-2 receptors using atropine (10(-5) M) increased acetylcholine release. After the M-2 receptors were blocked there was no difference in acetylcholine release between control and dexamethasone-treated cultures. M-2 receptor gene expressionwas increased by more than fivefold in dexamethasone-treated cultures. Immunostaining of dexamethasone-treated neurons demonstrated more intense staining, Thus, decreased vagally mediated reflex bronchoconstriction after glucocorticoid treatment may be the result on increased M-2 receptor expression and function as well as increased degradation of acetylcholine by cholinesterase.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/11/20 alle ore 20:29:21