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Titolo:
Pharmacological evidence for capacitative Ca2+ entry in cannulated and pressurized skeletal muscle arterioles
Autore:
Potocnik, SJ; Hill, MA;
Indirizzi:
RMIT Univ, Sch Med Sci, Div Biosci, Microvasc Biol Grp, Bundoora, Vic 3083, Australia RMIT Univ Bundoora Vic Australia 3083 Grp, Bundoora, Vic 3083, Australia
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 2, volume: 134, anno: 2001,
pagine: 247 - 256
SICI:
0007-1188(200109)134:2<247:PEFCCE>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE; CALCIUM-ENTRY; 2-AMINOETHOXYDIPHENYL BORATE; MYOGENIC RESPONSIVENESS; SARCOPLASMIC-RETICULUM; INOSITOL TRISPHOSPHATE; AGONIST STIMULATION; INTRACELLULAR CA2+; ENDOTHELIAL-CELLS; CHANNELS;
Keywords:
myogenic reactivity; arteriolar smooth muscle; capacitative Ca2+ entry; IP3 receptor; cell signalling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Hill, MA RMIT Univ, Sch Med Sci, Div Biosci, Microvasc Biol Grp, Plentry Rd, Bundoora, Vic 3083, Australia RMIT Univ Plentry Rd Bundoora Vic Australia 3083 3083, Australia
Citazione:
S.J. Potocnik e M.A. Hill, "Pharmacological evidence for capacitative Ca2+ entry in cannulated and pressurized skeletal muscle arterioles", BR J PHARM, 134(2), 2001, pp. 247-256

Abstract

1 Arteriolar myogenic tone shows a marked dependency on extracellular Ca-2(+). The contribution played by mechanisms such as intracellular Ca2 + release and capacitative entry, however, are less certain. The present studiesaimed to demonstrate functional evidence for involvement of such mechanisms in myogenic tone and reactivity.2 Single cremaster arterioles were denuded of endothelium, pressurized under no-flow conditions and loaded with fura 2-AM for measurement of changes in intracellular Ca-2 ' [Ca2 +](i). The cell permeable, putative, IP3 receptor antagonist 2APB (2 aminoethoxydiphenyl borate) was used to determine the possible role Of IP3 receptor-mediated mechanisms in arteriolar myogenic tone and reactivity.3 Arterioles dilated in response to increasing concentrations of 2APB (1 -300 muM) without a concomitant change in global [Ca2 +](i). Also 2APB (50 muM) completely inhibited the myogenic constriction in response to a step change in luminal pressure (50 - 120 mmHg) with no apparent effect on pressure-mediated increases in [Ca2 +](i). 2APB markedly attenuated the constrictor response and [Ca2 +](i) increase stimulated by phenylephrine but not KC1.4 Capacitative Ca2 + influx in arterioles was demonstrated either by re-addition of extracellular [Ca2 +] following pre-treatment with 1 or 10 muM nifedipine in Ca2 + free buffer or exposure of vessels to thapsigargin (1 muM) to induce store depletion. In both cases 2APB inhibited the increase in [Ca2 +](i). Capacitative Ca2 + entry showed an inverse relationship with intraluminal pressure over the range 10 - 120 mmHg.5 Consistent with an effect on a Ca2 + entry pathway, 2APB had no effect on intracellular (caffeine releasable) Ca2 + stores while decreasing the rate of Mn2 + quench of fura 2 fluorescence.6 The results provide functional evidence for capacitative Ca2 + entry in intact arteriolar smooth muscle. The effectiveness of 2APB in inhibiting both non-voltage gated Ca2 + entry and responsiveness to an acute pressure step is consistent with the involvement of an axis involving IP3-mediated andor capacitative Ca2 + entry mechanisms in myogenic reactivity. Given the lack of effect of 2APB on pressure-induced changes in global [Ca2 +](i) it is suggested that such mechanisms participate on a localized level to couplethe myogenic stimulus to contraction.

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Documento generato il 02/07/20 alle ore 21:48:11