Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Intestinal ion transport in NKCC1-deficient mice
Autore:
Grubb, BR; Lee, E; Pace, AJ; Koller, BH; Boucher, RC;
Indirizzi:
Univ N Carolina, Cyst Fibrosis Pulm Res & Treatment Ctr, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 t Ctr, Chapel Hill, NC 27599 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
fascicolo: 4, volume: 279, anno: 2000,
pagine: G707 - G718
SICI:
0193-1857(200010)279:4<G707:IITINM>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT DISTAL COLON; HCO3 SECRETION; BICARBONATE SECRETION; CYSTIC-FIBROSIS; COTRANSPORT; SODIUM; MOUSE; EXCHANGE; MUCOSA; CELLS;
Keywords:
sodium-potassium-chlorine ion cotransporter; chloride secretion; bicarbonate secretion; jejunum; cecum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Grubb, BR Univ N Carolina, Cyst Fibrosis Pulm Res & Treatment Ctr, 7011 Thurston Bowles Bldg,CB 7248, Chapel Hill, NC 27599 USA Univ N Carolina 7011 Thurston Bowles Bldg,CB 7248 Chapel Hill NC USA 27599
Citazione:
B.R. Grubb et al., "Intestinal ion transport in NKCC1-deficient mice", AM J P-GAST, 279(4), 2000, pp. G707-G718

Abstract

The Na+-K+-2Cl(-) cotransporter (NKCC1) located on the basolateral membrane of intestinal epithelia has been postulated to be the major basolateral Cl- entry pathway. With targeted mutagenesis, mice deficient in the NKCC1 protein were generated. The basal short-circuit current did not differ between normal and NKCC1 -/- jejuna. In the -/- jejuna, the forskolin response (22 mu A/cm(2); bumetanide insensitive) was significantly attenuated comparedwith the bumetanide-sensitive response (52 mu A/cm(2)) in normal tissue. Ion-replacement studies demonstrated that the forskolin response in the NKCC1 -/- jejuna was HCO3- dependent, whereas in the normal jejuna it was independent of the HCO3- concentration in the buffer. NKCC1 -/- ceca exhibited aforskolin response that did not differ significantly from that of normal ceca, but unlike that of normal ceca, was bumetanide insensitive. Ion-substitution studies suggested that basolateral HCO3- as well as Cl- entry (via non-NKCC1) paths played a role in the NKCC1 -/- secretory response. In contrast to cystic fibrosis mice, which lack both basal and stimulated Cl- secretion and exhibit severe intestinal pathology, the absence of intestinal pathology in NKCC1 -/- mice likely reflects the ability of the intestine to secrete HCO3- and Cl- by basolateral entry mechanisms independent of NKCC1.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 05:13:47