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Titolo:
INVOLVEMENT OF K-NAME AND INDOMETHACIN RESISTANT PART OF ADENOSINE-5'-O-(2-THIODIPHOSPHATE)-INDUCED RELAXATION OF PANCREATIC VASCULAR BED( CHANNEL PERMEABILITY CHANGES IN THE L)
Autore:
HILLAIREBUYS D; CHAPAL J; LINCK N; BLAYAC JP; PETIT P; LOUBATIERESMARIANI MM;
Indirizzi:
FAC MED MONTPELLIER,PHARMACOL LAB,UPRES EA 1677,BLVD HENRI IV F-34060MONTPELLIER 01 FRANCE
Titolo Testata:
British Journal of Pharmacology
fascicolo: 1, volume: 124, anno: 1998,
pagine: 149 - 156
SICI:
0007-1188(1998)124:1<149:IOKAIR>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION; PERFUSED MESENTERIC-ARTERIES; SMOOTH-MUSCLE CELLS; SENSITIVE POTASSIUM CHANNELS; NITRIC-OXIDE; PHYSIOLOGICAL SIGNIFICANCE; HEPATIC-ARTERY; RABBIT; ACETYLCHOLINE; ATP;
Keywords:
PANCREATIC VASCULAR BED; ADP-BETA-S; POTASSIUM CHANNELS; P2-RECEPTORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
D. Hillairebuys et al., "INVOLVEMENT OF K-NAME AND INDOMETHACIN RESISTANT PART OF ADENOSINE-5'-O-(2-THIODIPHOSPHATE)-INDUCED RELAXATION OF PANCREATIC VASCULAR BED( CHANNEL PERMEABILITY CHANGES IN THE L)", British Journal of Pharmacology, 124(1), 1998, pp. 149-156

Abstract

1 We have previously demonstrated that adenosine-5'-O-(2-thiodiphosphate) (ADP beta S), a potent P2Y-purinoceptor agonist, relaxed pancreatic vasculature not only through prostacyclin (PGI(2)) and nitric oxide(NO) release from the endothelium but also through other mechanism(s). In this study, we investigated the effects of an inhibitor of the Na/K+ pump, of ATP-sensitive K+ (K-ATP) channels and of small (SKCa) orlarge (BKCa) conductance Ca2+-activated K+ channels. Experiments wereperformed at basal tone and during the inhibition of NO synthase and cyclo-oxygenase. 2 In control conditions, ADP beta S (15 mu M) inducedan initial transient vasoconstriction followed by a progressive and sustained vasodilatation. In the presence of N omega-nitro-L-arginine methyl ester (L-NAME, 200 mu M) the transient vasoconstriction was reversed into a one minute vasodilator effect, which was then followed by a progressive and sustained vasodilatation similar to that observed with ADP beta S alone. The addition of indomethacin (10 mu M) did not significantly modify the profile of ADP beta S-induced vasodilatation. 3Ouabain (100 mu M) decreased basal pancreatic flow rate and did not modify ADP beta S-induced relaxation. This inhibitor of the Na+/K+ pumpincreased the pancreatic vasoconstriction induced by L-NAME or by thecn-administration of L-NAME and indomethacin. Ouabain did not modify either the L-NAME or the L-NAME/indomethacin resistant part of the ADPbeta S vasodilatation. 4 The K-ATP inhibitor tolbutamide (185 mu M) did not significantly modify basal pancreatic flow rate and ADP beta S-induced relaxation. This inhibitor which did not change L-NAME-inducedvasoconstriction, significantly diminished the L-NAME resistant part of ADP beta S-induced vasodilatation. Tolbutamide intensified the vasoconstriction induced by the co-administration of L-NAME and indomethacin. In contrast, the L-NAME/indomethacin resistant part of ADP beta S vasodilatation was not changed by the closure of K-ATP. 5 The SKCa inhibitor apamin (0.1 mu M) did not significantly change pancreatic vascular resistance whatever the experimental conditions (in the absence orin presence of L-NAME or L-NAME/indomethacin). In the presence of L-NAME, the closure of SKCa channels changed the one minute vasodilator effect of ADP beta S into a potent vasoconstriction and thereafter modified only the beginning of the second part of the L-NAME-resistant part of the ADP beta S-induced vasodilatation. In contrast, the L-NAME/indomethacin resistant part of ADP beta S-induced relaxation remained unchanged in the presence of apamin. 6 Charybdotoxin (0.2 mu M), an inhibitor of BKCa, increased pancreatic vascular resistance in the presence of L-NAME/indomethacin. In the presence of L-NAME, the closure of BKCa channels reversed the one minute vasodilator effect of AD beta PS into a potent vasoconstriction and drastically diminished the sustainedvasodilatation. In contrast the L-NAME/indomethacin resistant part ofADP beta S-induced relaxation was not modified by the presence of charybdotoxin. Under L-NAME/indomethacin/charybdotoxin/apamin infusions, ADP beta S evoked a drastic and transient vasoconstriction reaching a maximum at the second minute, which was followed by a sustained increase in the flow rate throughout the ADP beta S infusion. The maximal vasodilator effect of ADP beta S observed was not modified by the addition of apamin. 7 The results suggest that the L-NAME-resistant relaxation induced by ADP beta S in the pancreatic vascular bed involves activation of BKCa, K-ATP and to a lesser extent of SKCa channels, but the L-NAME/indomethacin resistant part of ADP beta S-induced relaxation isinsensitive to the closure of K-ATP, SKCa and BKCa channels.

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Documento generato il 07/07/20 alle ore 12:09:42