Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
MECHANISMS OF STRETCH-INDUCED CHANGES IN [CA2- ROLE OF INCREASED TROPONIN-C AFFINITY AND STRETCH-ACTIVATED ION CHANNELS(](I) IN RAT ATRIAL MYOCYTES )
Autore:
TAVI P; HAN CL; WECKSTROM M;
Indirizzi:
UNIV OULU,DEPT PHYSIOL,KAJAANINTIE 52A FIN-90220 OULU FINLAND UNIV OULU,DEPT PHYSIOL FIN-90220 OULU FINLAND UNIV OULU,DEPT PHYS SCI,DIV BIOPHYS FIN-90220 OULU FINLAND UNIV OULU,BIOCTR OULU FIN-90220 OULU FINLAND
Titolo Testata:
Circulation research
fascicolo: 11, volume: 83, anno: 1998,
pagine: 1165 - 1177
SICI:
0009-7330(1998)83:11<1165:MOSCI[>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
PIG VENTRICULAR MYOCYTES; INTRACELLULAR CALCIUM TRANSIENTS; CULTURED CHICK HEART; GUINEA-PIG; CARDIAC-MUSCLE; DEPENDENT CHANGES; DYNAMIC-MODEL; MECHANOELECTRICAL FEEDBACK; SARCOMERE-LENGTH; PAPILLARY-MUSCLE;
Keywords:
STRETCH; MYOCYTE; FRANK-STARLING; CA2+; ACTION POTENTIAL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
79
Recensione:
Indirizzi per estratti:
Citazione:
P. Tavi et al., "MECHANISMS OF STRETCH-INDUCED CHANGES IN [CA2- ROLE OF INCREASED TROPONIN-C AFFINITY AND STRETCH-ACTIVATED ION CHANNELS(](I) IN RAT ATRIAL MYOCYTES )", Circulation research, 83(11), 1998, pp. 1165-1177

Abstract

To study the effects of stretch on the function of rat left atrium, we recorded contraction force, calcium transients, and intracellular action potentials (APs) during stretch manipulations. The stretch of theatrium was controlled by intra-atrial pressure. The Frank-Starling behavior of the atrium was manifested as a biphasic increase of the contraction force after increasing the stretch level. The development of the contraction force after step increase of the stretch (intra-atrial pressure from 1 to 3 mm Hg) was accompanied by the increase in the amplitude of the calcium transients (P<0.05, n=4) and decrease in the time constant of the Ca2+ transient decay. The APs of the individual myocytes were also affected by stretch; the duration of the AP was decreased at positive voltages (AP duration at 15% repolarization level, P<0.001; n = 13) and increased at negative voltages (AP duration at 90% repolarization level, P<0.01; n=13). To study the mechanisms causing these changes we developed a mathematical model describing [Ca2+](i) and electrical behavior of single rat atrial myocytes. Stretch was simulated in the model by increasing the troponin (TnC) sensitivity and/or applying a stretch-activated (SA) calcium influx. We mimicked the Ca2+ influx by introducing a nonselective cationic conductance, the SA channels, into the membrane. Neither of the 2 plausible mechanosensors (TnCor SA channels) alone could produce similar changes in the Ca2+ transients or APs as seen in the experiments. The model simulated the effects of stretch seen in experiments best when both the TnC affinity and the SA conductance activation were applied simultaneously. The SA channel activation led to gradual augmentation of Ca2+ transients, which modulated the APs through increased Na+/Ca2+-exchanger inward current. The role of TnC affinity change was to modulate the Ca2+ transients, stabilize the diastolic [Ca2+](i) and presumably to produce the immediate increase of the contraction force after stretch seen in experiments. Furthermore, we found that the same mechanism that caused the normalphysiological responses to stretch could also generate arrhythmogenicafterpotentials at high stretch levels in the model.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 00:21:21