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Titolo:
M(1) MUSCARINIC MECHANISMS REGULATE INTESTINAL-PHASE GALLBLADDER PHYSIOLOGY IN HUMANS
Autore:
NELSON DK; GLASBRENNER B; DAHMEN G; RIEPL RL; MALFERTHEINER P; ADLER G;
Indirizzi:
UNIV ROCHESTER,GENESSEE HOSP,ISAAC GORDEN CTR DIGEST DIV & NUTR,224 ALEXANDER ST ROCHESTER NY 14607 UNIV MUNICH,MED KLIN INNENSTADT D-8000 MUNICH GERMANY UNIV ULM D-89069 ULM GERMANY UNIV MAGDEBURG D-39106 MAGDEBURG GERMANY
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 5, volume: 34, anno: 1996,
pagine: 824 - 830
SICI:
0193-1857(1996)34:5<824:MMMRIG>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
PANCREATIC-POLYPEPTIDE; RECEPTOR SUBTYPES; CHOLINERGIC DEPENDENCE; SMOOTH-MUSCLE; DOSE-RESPONSE; CHOLECYSTOKININ; CONTRACTION; PIRENZEPINE; SECRETION; ANTAGONIST;
Keywords:
BILIARY PHYSIOLOGY; CHOLINERGIC; CHOLECYSTOKININ; PANCREATIC POLYPEPTIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
D.K. Nelson et al., "M(1) MUSCARINIC MECHANISMS REGULATE INTESTINAL-PHASE GALLBLADDER PHYSIOLOGY IN HUMANS", American journal of physiology: Gastrointestinal and liver physiology, 34(5), 1996, pp. 824-830

Abstract

The contribution of muscarinic receptor subtypes to biliary control mechanisms is unclear. We investigated stimulated gallbladder function and release of associated hormones during M(1)-receptor blockade. Following a double-blind, randomized, crossover protocol, healthy volunteers each received placebo and telenzepine, a selective M(1)-receptor antagonist, as 2-h background infusion. Gallbladder contraction (by ultrasonography), bilirubin output, and release of cholecystokinin (CCK) and pancreatic polypeptide (PP) were assessed during increasing doses of endogenous (intraduodenal nutrient) and exogenous (hormonal) stimulation. All parameters were stimulated in a dose-dependent manner on placebo days. Contractile and secretory responses to low-dose caerulein (CCK analogue) were inhibited by 60-80% under telenzepine, whereas high-dose (supraphysiological) stimulation overrode this effect. Similar inhibition was achieved during nutrient stimulation. CCK plasma levels rose during endogenous and exogenous stimulation but were unaffected by M(1) blockade, whereas stimulated PP release was completely inhibited (> 100% decrease), reflecting suppressed vagal tone. Selective M(1)-receptor blockade inhibits the physiological response of the gallbladder in humans; this effect cannot be attributed to suppressed CCK release. Our findings support the hypothesis that CCK acts at the gallbladder via cholinergic nerves under physiological conditions. Viewed with our previous observations, nonselective antagonism of biliary functionby atropine is primarily mediated through M(1) muscarinic pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 03:26:44