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Titolo:
ANTAGONISM OF LEVCROMAKALIM BY IMIDAZOLINE-DERIVATIVES AND GUANIDINE-DERIVATIVES IN RAT PORTAL-VEIN - INVOLVEMENT OF THE DELAYED RECTIFIER
Autore:
IBBOTSON T; EDWARDS G; WESTON AH;
Indirizzi:
UNIV MANCHESTER,DEPT PHYSIOL SCI,SMOOTH MUSCLE RES GRP MANCHESTER M139PT LANCS ENGLAND UNIV MANCHESTER,DEPT PHYSIOL SCI,SMOOTH MUSCLE RES GRP MANCHESTER M139PT LANCS ENGLAND
Titolo Testata:
British Journal of Pharmacology
fascicolo: 4, volume: 110, anno: 1993,
pagine: 1556 - 1564
SICI:
0007-1188(1993)110:4<1556:AOLBIA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE K+ CHANNELS; PANCREATIC BETA-CELLS; SMOOTH-MUSCLE CELLS; GUINEA-PIG; ALPHA-2-ADRENERGIC RECEPTOR; CROMAKALIM; GLIBENCLAMIDE; PHENTOLAMINE; INHIBITION; BRL-38227;
Keywords:
LEVCROMAKALIM; CLONIDINE; PHENTOLAMINE; GUANABENZ; CIRAZOLINE; ANTAZOLINE; RAT PORTAL VEIN; VOLTAGE-CLAMP; NON-ADRENOCEPTOR IMIDAZOLINE BINDING SITE; POTASSIUM CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
T. Ibbotson et al., "ANTAGONISM OF LEVCROMAKALIM BY IMIDAZOLINE-DERIVATIVES AND GUANIDINE-DERIVATIVES IN RAT PORTAL-VEIN - INVOLVEMENT OF THE DELAYED RECTIFIER", British Journal of Pharmacology, 110(4), 1993, pp. 1556-1564

Abstract

1 In rat whole portal veins, guanabenz (100 nm to 10 muM) and antazoline (100 nm to 100 muM) each increased the amplitude, frequency and duration of spontaneous contractions. In addition, guanabenz (30 muM) and antazoline (30 muM) each antagonized the ability of levcromakalim (3nm to 10 muM) to inhibit the spontaneous contractions of this tissue.2 Whole-cell voltage-clamp recordings were made from freshly-isolatedrat portal vein cells dispersed by a collagenase/pronase enzyme treatment. The ability of several agents (antazoline, cirazoline, clonidine, guanabenz and phentolamine, each containing an imidazoline or guanidine moiety), to modulate potassium (K) currents and to inhibit the actions of levcromakalim was investigated. 3 Antazoline, cirazoline, clonidine, guanabenz and phentolamine (each at a concentration of 30 muM) had little effect on-control non-inactivating currents but inhibited the delayed-rectifier current, I(K(V)). 4 Leveromakalim (1 muM) induceda non-inactivating current, I(K(ATP)), and also inhibited the delayedrectifier current, I(K(V)). 5 Glibenclamide (I muM) had no effect on control delayed rectifier or non-inactivating currents, but it inhibited the simultaneous induction of I(K(ATP)) and reduction of I(K(V)) produced by levcromakalim (1 muM). 6 Antazoline, cirazoline, clonidine and guanabenz (each at a concentration of 30 muM) prevented the induction of I(K(ATP)) by levcromakalim (1 muM). Phentolamine (30 muM) and clonidine (30 muM) each inhibited the I(K(ATP)) generated by levcromakalim (1 muM). 7 It is concluded that a variety of agents which possess either an imidazoline (antazoline, cirazoline, clonidine and phentolamine) or a guanidine (guanabenz) moiety within their structure inhibit the delayed rectifier current, I(K(v)). This action may thus be mediated via a so-called non-adrenoceptor imidazoline binding site. Furthermore, the ability of these ligands to inhibit I(K(V)) and to antagonize both the induction of I(K(ATP)) and the vasorelaxation produced by levcromakalim is consistent with the view that the channel (K(ATP)) whichunderlies I(K(ATP)) is a voltage-insensitive state of the delayed rectifier K-channel (K(V)).

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Documento generato il 06/07/20 alle ore 09:01:11