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Titolo:
EFFECT OF FORSKOLIN ON ENDOTHELIN-INDUCED PHOSPHOINOSITIDE HYDROLYSISAND CALCIUM MOBILIZATION IN CULTURED CANINE TRACHEAL SMOOTH-MUSCLE CELLS
Autore:
YANG CM; PAN SL; CHIU CT; LIN CC; HSU M;
Indirizzi:
CHANG GUNG UNIV,COLL MED,DEPT PHARMACOL,CELLULAR & MOL PHARMACOL LAB,259 WEN HWA 1 RD TAYUAN TAIWAN
Titolo Testata:
Journal of autonomic pharmacology
fascicolo: 4, volume: 18, anno: 1998,
pagine: 213 - 221
SICI:
0144-1795(1998)18:4<213:EOFOEP>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
INOSITOL PHOSPHOLIPID HYDROLYSIS; DEPENDENT PROTEIN-KINASE; 2ND MESSENGER SYSTEMS; CYCLIC-AMP LEVELS; VASOCONSTRICTOR PEPTIDE; SIGNAL-TRANSDUCTION; ADENYLATE-CYCLASE; TURNOVER; INHIBITION; CAMP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
C.M. Yang et al., "EFFECT OF FORSKOLIN ON ENDOTHELIN-INDUCED PHOSPHOINOSITIDE HYDROLYSISAND CALCIUM MOBILIZATION IN CULTURED CANINE TRACHEAL SMOOTH-MUSCLE CELLS", Journal of autonomic pharmacology, 18(4), 1998, pp. 213-221

Abstract

1 The effects of increase in intracellular adenosine 3':5'-cyclic monophosphate (cAMP) on endothelin-l (ET-1)-induced generation of inositol phosphates (IPs) and increase in intracellular Ca2+ ([Ca2+](i)) wereinvestigated in canine cultured tracheal smooth muscle cells (TSMCs).2 Pretreatment of TSMCs with either cholera toxin (CTX; 10 mu g ml(-1), 4 h), forskolin (10 mu M, 30 min), or dibutyryl cAMP (1 mM, 30 min)inhibited ET-l-stimulated Ca2+ mobilization (by 23 +/- 5%, n = 8) andIPs accumulation (by 32 +/- 6%, n = 4). While after treatment with forskolin for 24 h, the cells retained the ability to respond to ET-l-induced Ca2+ mobilization to the same extent as the control group. 3 Forskolin (1-100 mu M) inhibited the ET-l-induced increase in [Ca2+](i), but the lower concentrations had little effect on this response. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the right of the concentration-response curve of ET-1 without changing the -logEC(50) values. 4 The water-soluble forskolin analogue L-858051, 7-deacetyl-7 beta-(gamma-N-methylpiperazino)-butyryl forskolin, significantly inhibited ET-l-stimulated IPs accumulation. In contrast, the addition of 1,9-dideoxy forskolin, an inactive analogue of forskolin, had little effect on stimulated responses. Moreover, SQ-22536, 9-(tetrahydro-2-furanyl)-9H-purin-6-amine, an inhibitor of adenylate cyclase, and both H-89, N-(2-aminoethyl)-5-isoquinolinesulfonamide, and HA-1004, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide, inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit ET-l-induced IPs accumulation. These results suggest that activation of cAMP/PKA was involved in these inhibitory effects of forskolin. 5 The locus of this inhibition of forskolin treatment on AlF4--stimulated IPs accumulation was investigated in canine TSMCs. The AlF4--induced IPs accumulation was inhibited by forskolin, supporting that G protein(s) are directly activated by AkF(4)(-) and uncoupled to phospholipase C by forskolin treatment. 4 We conclude that cAMP elevating agents inhibit ET-l-stimulated generationof IPs and Ca2+ mobilization in canine cultured TSMCs. Since generation of IPs and increases in [Ca2+](i) are very early events in the activation of ET-1 receptors, attenuation of these events by cAMP elevating agents might well contribute to the inhibitory effect of cAMP on tracheal smooth muscle function.

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Documento generato il 05/04/20 alle ore 05:54:36