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Titolo:
Effects of mibefradil and nifedipine on arteriolar myogenic responsivenessand intracellular Ca2+
Autore:
Potocnik, SJ; Murphy, TV; Kotecha, N; Hill, MA;
Indirizzi:
RMIT Univ, Dept Human Biol & Movement Sci, Microvasc Biol Grp, Bundoora, Vic 3083, Australia RMIT Univ Bundoora Vic Australia 3083 Grp, Bundoora, Vic 3083, Australia Monash Univ, Dept Physiol, Clayton, Vic 3168, Australia Monash Univ Clayton Vic Australia 3168 siol, Clayton, Vic 3168, Australia
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 6, volume: 131, anno: 2000,
pagine: 1065 - 1072
SICI:
0007-1188(200011)131:6<1065:EOMANO>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT CEREBRAL-ARTERIES; SMOOTH-MUSCLE CELLS; CALCIUM CHANNELS; T-TYPE; TONE; INHIBITION; PRESSURE; ANTAGONIST; RO-40-5967; MECHANISM;
Keywords:
Ca2+ entry; arterioles; myogenic tone; myogenic response; intracellular Ca2+; membrane potential; smooth muscle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Hill, MA RMIT Univ, Dept Human Biol & Movement Sci, Microvasc Biol Grp, Plenty Rd, Bundoora, Vic 3083, Australia RMIT Univ Plenty Rd Bundoora Vic Australia 3083 c 3083, Australia
Citazione:
S.J. Potocnik et al., "Effects of mibefradil and nifedipine on arteriolar myogenic responsivenessand intracellular Ca2+", BR J PHARM, 131(6), 2000, pp. 1065-1072

Abstract

1 Ca2+ entry mechanisms underlying spontaneous arteriolar tone and acute myogenic reactivity remain uncertain. Those studies aimed to compare the effects of nifedipine and the putative T-channel blocker, mibefradil, on arteriolar myogenic responsiveness and intracellular Ca2+ (Ca-i(2+)).2 First order cremaster muscle arterioles (1A) were isolated from rats, cannulated, pressurized to 70 mmHg in the absence of intraluminal how, and mechanical responses studied by video microscopy. The Ca-i(2+) was measured using fluorescence imaging of Fura 2 loaded arterioles.3 Both nifedipine and mibefradil showed dose-dependent inhibition of spontaneous myogenic tone (at 70 mmHg: pEC(50) 7.04+/-0.17 vs 6.65+/-0.20 respectively, n=6 for both, n.s.) and KCl-induced vasoconstriction (at 70 mmHg; pEC(50), 6.93+/-0.38 vs 6.45+/-0.27 respectively, n=6 for both, n.s.).4 In arterioles maintained at 50 mmHg, nifedipine (10(-7) and 10(-5) M) caused a concentration dependent, reduction in Ca-i(2+), however, mibefradil (10(-7) and 10(-5) M) had no effect. Furthermore nifedipine significantly attenuated the increase in Ca-i(2+) associated with an acute pressure step (50-120 mmHg) whereas mibefradil was considerably less effective.5 Mibefradil (10 M-7) significantly attenuated contractile responses to 60mM KCl without altering the KCl-incluced increase in Ca-i(+2), in contrastto nifedipine (10(-7) M) which reduced both Ca-i(2+) and contraction.6 Membrane potential of arterioles with spontaneous myogenic tone (70mmHg)was -41.5+/-1.0 mV. Nifedipine (10(-7) or 10(-5) M ) had no effect on membrane potential, however mibefradil (10(-5 M)) caused significant depolarization.7 In summary, both mibefradil and nifedipine inhibit arteriolar spontaneous tone and acute myogcnic reactivity. While there may be overlap in the mechanisms by which these agents inhibit tone, differences in effects on membrane potential and intracellular Ca2+ levels suggest mibefradil exhibits actions other than blockade of Ca2+ entry in skeletal muscle arterioles.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 00:46:14