PHOSPHOLIPASE-C-INDUCED ANION SECRETION AND ITS INTERACTION WITH CARBACHOL IN THE RAT COLONIC MUCOSA

被引:38
作者
DIENER, M [1 ]
EGLEME, C [1 ]
RUMMEL, W [1 ]
机构
[1] UNIV SAARLAND,INST MED BIOCHEM,W-6650 HOMBURG,GERMANY
关键词
PHOSPHOLIPASE-C; CL-SECRETION; CA2+; PROTEIN KINASE-C;
D O I
10.1016/0014-2999(91)90581-A
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Phospholipase C (PLC) from clostridium perfringens induced a biphasic increase in short-circuit current (Isc) in the rat colon. The Isc rose rapidly to a transient peak, before it increased again to a plateau lasting for several hours. Ion replacement experiments and sensitivity to furosemide or a Cl- channel blocker indicated that PLC induced Cl- secretion. The first peak was suppressed by indomethacin, indicating mediation by prostaglandins. In contrast, the second phase was only partially sensitive to the cyclooxygenase blocker. The long-time action of PLC was dependent on intra- and extracellular Ca2+, although PLC did not induce an increase in the intracellular Ca2+ concentration of the enterocytes. The effect of PLC was blocked by the protein kinase inhibitor, staurosporine. Carbachol, when added during the second phase of the PLC response, induced a 'paradox' change in Isc: a rapid, transient increase in Isc was followed by a long-lasting decrease. This inhibition of the PLC response was more pronounced after elevation of the external Ca2+ concentration. A Ca2+ ionophore, ionomycin, and a Ca2+ channel activator, BAY K 8644, also inhibited the PLC response. The results suggest dual dependence of the action of PLC on the intracellular Ca2+ concentration.
引用
收藏
页码:267 / 276
页数:10
相关论文
共 44 条
[1]  
ABDELLATIF AA, 1986, PHARMACOL REV, V38, P227
[2]   SUBMUCOSAL PLEXUS AND ELECTROLYTE TRANSPORT ACROSS RAT COLONIC MUCOSA [J].
ANDRES, H ;
BOCK, R ;
BRIDGES, RJ ;
RUMMEL, W ;
SCHREINER, J .
JOURNAL OF PHYSIOLOGY-LONDON, 1985, 364 (JUL) :301-+
[3]   FORSKOLIN INDUCED CHLORIDE SECRETION ACROSS THE ISOLATED MUCOSA OF RAT COLON DESCENDENS [J].
BRIDGES, RJ ;
RUMMEL, W ;
SIMON, B .
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, 1983, 323 (04) :355-360
[4]   CELLULAR MECHANISM OF INTESTINAL PERMEABILITY ALTERATIONS PRODUCED BY CHELATION DEPLETION [J].
CASSIDY, MM ;
TIDBALL, CS .
JOURNAL OF CELL BIOLOGY, 1967, 32 (03) :685-+
[6]   MECHANISM OF ARACHIDONIC ACID-INDUCED CA-2+ MOBILIZATION FROM RAT-LIVER MICROSOMES [J].
CHAN, KM ;
TURK, J .
BIOCHIMICA ET BIOPHYSICA ACTA, 1987, 928 (02) :186-193
[7]   PHOSPHOLIPASE-A2 - FUNCTION AND PHARMACOLOGICAL REGULATION [J].
CHANG, J ;
MUSSER, JH ;
MCGREGOR, H .
BIOCHEMICAL PHARMACOLOGY, 1987, 36 (15) :2429-2436
[8]   PROTEIN KINASE-C MEDIATES CHOLINERGICALLY REGULATED PROTEIN-PHOSPHORYLATION IN A CL--SECRETING EPITHELIUM [J].
COHN, JA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (02) :C227-C233
[9]   PATTERNS OF PROSTAGLANDIN SYNTHESIS AND DEGRADATION IN ISOLATED SUPERFICIAL AND PROLIFERATIVE COLONIC EPITHELIAL-CELLS COMPARED TO RESIDUAL COLON [J].
CRAVEN, PA ;
DERUBERTIS, FR .
PROSTAGLANDINS, 1983, 26 (04) :583-604