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Titolo:
Intracellular acidosis modulates the stretch-induced changes in E-C coupling of the rat atrium
Autore:
Tavi, P; Han, C; Weckstrom, M;
Indirizzi:
Univ Oulu, Dept Physiol, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 lu, Dept Physiol, SF-90220 Oulu, Finland Univ Oulu, Bioctr, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 niv Oulu, Bioctr, SF-90220 Oulu, Finland Univ Oulu, Dept Phys Sci, Div Biophys, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 Sci, Div Biophys, SF-90220 Oulu, Finland
Titolo Testata:
ACTA PHYSIOLOGICA SCANDINAVICA
fascicolo: 3, volume: 167, anno: 1999,
pagine: 203 - 213
SICI:
0001-6772(199911)167:3<203:IAMTSC>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAMMALIAN CARDIAC-MUSCLE; FERRET VENTRICULAR MUSCLE; GUINEA-PIG; DEPENDENT CHANGES; SARCOPLASMIC-RETICULUM; CALCIUM TRANSIENTS; MOLECULAR-BASIS; CYTOSOLIC CA2+; LENGTH CHANGES; HEART-MUSCLE;
Keywords:
action potential; contraction; heart; intracellular calcium; ischaemia; myocyte; Na+/Ca2+ exchanger; propionic acid;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Tavi, P Univ Oulu, Dept Physiol, Kajaanintie 52 A, SF-90220 Oulu, Finland Univ Oulu Kajaanintie 52 A Oulu Finland SF-90220 20 Oulu, Finland
Citazione:
P. Tavi et al., "Intracellular acidosis modulates the stretch-induced changes in E-C coupling of the rat atrium", ACT PHYSL S, 167(3), 1999, pp. 203-213

Abstract

By inducing a small reduction of the intracellular pH (0.18 units) with 20mmol L-1 propionate we demonstrated that acidification changed the responses of isolated rat atria to stretch. Stretch (increase of the intra-atrial pressure) in normal pH increased the Ca2+ transients' amplitude (Indo-1 fluorescence) from 0.26 +/- 0.09 in 1 mmHg to 0.36 +/- 0.13 in 4 mmHg (P < 0.05, n = 6), without affecting the diastolic [Ca2+](i) level (n.s. n = 6). The changes in Ca2+ balance during stretch were accompanied by a biphasic increase in the contraction force. Five minutes of continuous stretch increased the action potential duration (APD(90%), P < 0.01, n = 13) and decreased the APD(15%) (P < 0.001, n = 13). During acidosis, the stretch-induced increase of the Ca2+ transient amplitude (0.4 +/- 0.13 vs. 0.3 +/- 0.08, P < 0.05, n = 6) was accompanied by the increase of the diastolic [Ca2+](i) (1.16+/- 0.07, P < 0.05, n = 6) compared with non-acidotic control (1.06 +/- 0.06, n = 6). Acidic intracellular pH also inhibited the stretch-induced changes in the action potentials (n = 10) and slowed down the development of the contractile force during stretch. The results showed that acidosis modulates the mechanotransduction. It does this by interfering with the intracellular Ca2+ balance, inhibiting the Ca2+ extrusion mechanisms and reducing the Ca2+-buffering power of the cells. The physiological and pathological processes associated with stretch are therefore modulated by intracellular pH owing to its concerted effects on intracellular Ca2+ handling caused by a competitive inhibition of various Ca2+-binding molecules.

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Documento generato il 25/11/20 alle ore 01:27:40