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Titolo:
The inhibition of cholera toxin-induced 5-HT release by the 5-HT3 receptorantagonist, granisetron, in the rat
Autore:
Turvill, JL; Connor, P; Farthing, MJG;
Indirizzi:
St Batholomews & Royal London Sch Med & Dent, Digest Dis Res Ctr, London E1 2AD, England St Batholomews & Royal London Sch Med & Dent London England E1 2AD gland
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 5, volume: 130, anno: 2000,
pagine: 1031 - 1036
SICI:
0007-1188(200007)130:5<1031:TIOCT5>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED FLUID SECRETION; SMALL-INTESTINE; SUBMUCOSAL PLEXUS; 5-HYDROXYTRYPTAMINE; SEROTONIN; TRANSPORT; NEURONS; MODULATION; INVIVO; RABBIT;
Keywords:
cholera toxin; small intestine; water transport; 5-hydroxytryptamine; granisetron;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Turvill, JL St Batholomews & Royal London Sch Med & Dent, Digest Dis Res Ctr, Turner St, London E1 2AD, England St Batholomews & Royal London Sch Med& Dent Turner St London England E1 2AD
Citazione:
J.L. Turvill et al., "The inhibition of cholera toxin-induced 5-HT release by the 5-HT3 receptorantagonist, granisetron, in the rat", BR J PHARM, 130(5), 2000, pp. 1031-1036

Abstract

1 The secretagogue 5-hydroxytryptamine (5-MT) is implicated in the pathophysiology of cholera. 5-HT released from enterochromaffin cells after cholera toxin exposure is thought to activate non-neuronally (5-HT2 dependent) and neuronally (5-HT3 dependent) mediated water and electrolyte secretion. CT-secretion can be reduced by preventing the release of 5-MT.2 Enterochromaffin cells possess numerous receptors that, under basal conditions, modulate 5-HT release. These include basolateral 5-HT3 receptors, the activation of which is known to enhance 5-HT release.3 Until now, 5-HT3 receptor antagonists (e.g. granisetron) have been thought to inhibit cholera toxin-induced fluid secretion by blockading 5-HT3 receptors on secretory enteric neurones. Instead we postulated that they act by inhibiting cholera toxin-induced enterochromaffin cell degranulation.4 Isolated intestinal segments in anaesthetized male Wistar rats, pre-treated with granisetron 75 mu g kg(-1), lidoocaine 6 mg kg(-1) or saline, wereinstilled with a supramaximal dose of cholera toxin or saline. Net fluid movement was determined by small intestinal perfusion or gravimetry and small intestinal and luminal fluid 5-HT levels were determined by HPLC with fluorimetric detection.5 Intraluminal 5-HT release was proportional to the reduction in tissue 5-HT levels and to the onset of water and electrolyte secretion, suggesting that luminal 5-HT levels reflect enterochromaffin cell activity.6 Both lidocaine and granisetron inhibited fluid secretion. However, granisetron alone, and proportionately, reduced 5-HT release.7 The simultaneous inhibition of 5-HT release and fluid secretion by granisetron suggests that 5-HT release from enterochromaffin cells is potentiated by endogenous 5-MT, accentuated 5-HT release promotes cholera toxin-induced fluid secretion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 06:50:23