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Titolo:
A(2) ADENOSINE RECEPTORS IN MONGOLIAN GERBIL MIDDLE-EAR EPITHELIUM AND THEIR REGULATION OF CL- SECRETION
Autore:
FURUKAWA M; IKEDA K; OSHIMA T; SUZUKI H; YAMAYA M; SASAKI H; TAKASAKA T;
Indirizzi:
TOHOKU UNIV,SCH MED,DEPT OTORHINOLARYNGOL,AOBA KU,1-1 SEIRYO MACHI SENDAI MIYAGI 9808574 JAPAN TOHOKU UNIV,SCH MED,DEPT GERIATR MED,AOBA KU SENDAI MIYAGI 9808574 JAPAN
Titolo Testata:
Acta Physiologica Scandinavica
fascicolo: 1, volume: 163, anno: 1998,
pagine: 103 - 112
SICI:
0001-6772(1998)163:1<103:AARIMG>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSMEMBRANE CONDUCTANCE REGULATOR; RECTIFYING CHLORIDE CHANNELS; CYSTIC-FIBROSIS; CELL-LINE; MOLECULAR-CLONING; TRACHEAL EPITHELIUM; PROTEIN-KINASE; CYCLIC-AMP; CAMP; CFTR;
Keywords:
ADENOSINE; CAMP; CFTR; CHLORIDE SECRETION; MIDDLE EAR EPITHELIUM; SHORT-CIRCUIT CURRENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
M. Furukawa et al., "A(2) ADENOSINE RECEPTORS IN MONGOLIAN GERBIL MIDDLE-EAR EPITHELIUM AND THEIR REGULATION OF CL- SECRETION", Acta Physiologica Scandinavica, 163(1), 1998, pp. 103-112

Abstract

The present study investigates the effects of adenosine and its analogues on CI- secretion in primary cultures of gerbil middle ear epithelium. Short-circuit current (I-sc), an index of transepithelial active transport, was measured on the same cells cultured on porous filters. Baseline I-sc and transepithelial resistance were 27.0 +/- 0.7 mu A cm(-2) and 275 +/- 7 Omega cm(2), respectively (n = 178). Extracellular adenosine and its analogues elicited a sustained increase in I-sc whenadded to apical or basolateral surfaces. Both the A(2A) selective agonist -carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine and the A(2A)/A(2B) nonselective agonist 5'-(N-ethyl-carboxamido)adenosine(NECA) increased I-sc, but NECA was more effective than CGS21680. A(1) selective antagonist 8-cyclopentyl-1,3-dipropylxanthine did not reduce NECA-induced I-sc. These results suggest the presence of both APA anti A(2B) receptors. NECA did not stimulate a rise in the intracellular Ca2+ concentration ([Ca2+](i)) in single middle ear epithelial cellscultured on glass coverslips. Dibutyryl cAMP (dbcAMP) induced an initial transient increase in I-sc followed by the sustained plateau. Addition of dbcAMP also caused a transient increase in [Ca2+](i). The protein kinase A inhibitor, omocinnamylamino)ethyl]-5-isoquinolinesulfonamide, greatly reduced the increase in the I-sc responses to NECA. 1,2-Bis-(2-aminophenoxy)ethane N,N,N',N' tetraacetic acid-acetoxymethyl ester influenced neither the NECA-induced increase in I-sc nor the dbcAMP-induced sustained phase of I-sc, but greatly inhibited the dbcAMP-induced transient increase in I-sc(. ) Glibenclamide, a cystic fibrosis transmembrane conductance regulator (CFTR) channel inhibitor, reduced the NECA-induced I-sc. These results indicate that extracellular adenosine and its analogues activate the cAMP-protein kinase A system, but not intracellular Ca2+-dependent mechanisms, leading to Cl- secretion, possibly through the CFTR Cl- channels in the cultured gerbil middle ear epithelium.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:28:12