In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 279, No. 2 ( 2000-08-01), p. H798-H807
Kurzfassung:
Excitation-contraction (E-C) coupling was investigated in rat hearts 6 wk after induction of myocardial infarction (MI) by ligation of the left coronary artery. Heart weight was increased by 74% and left ventricular end-diastolic pressure was 23 ± 2 mmHg in MI compared with 8 ± 2 mmHg in sham-operated controls (Sham, P 〈 0.001). Cell shortening was measured in voltage-clamped myocytes at 36°C. In solutions where Cs + had been replaced by K + , the voltage dependence of contraction was sigmoidal between −20 and +100 mV in Sham and MI cells. Verapamil (20 μM) blocked L-type Ca 2+ current and reduced contraction in Sham cells by ∼50% ( P 〈 0.01) but did not decrease contraction significantly in MI cells at test potentials above +10 mV. Verapamil-insensitive contractions were blocked by Ni 2+ (5 mM). Na + /Ca 2+ exchange current was doubled in MI compared with Sham cells at test potentials between −20 and +80 mV ( P 〈 0.05), whereas mRNA and protein expression increased by 30–40%. Finally, voltage dependence of contraction was bell shaped in Na + -free solutions, but contraction was significantly increased in MI cells over a wider voltage range ( P 〈 0.05). The insensitivity to Ca 2+ channel block in MI cells may result from an increased contribution of the Na + /Ca + exchanger to triggering of E-C coupling. These results suggest significant changes in E-C coupling in the hypertrophy and failure that develop in response to extensive MI.
Materialart:
Online-Ressource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.2000.279.2.H798
Sprache:
Englisch
Verlag:
American Physiological Society
Publikationsdatum:
2000
ZDB Id:
1477308-9
SSG:
12
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