Résumé :
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Communication n° 678 Introduction : The development of coronary occlusion and vasospasm is related to the impairment of Ca2+ homeostasis occurring in several cardiomyopathies. The voltage-independent B-type Ca2+ channels have, in normal condition, activity which is responsible for a low level basal entry of calcium. They have been found to modulate apoptosis of cardiac myocytes by cross-talking with mitochondrial Ca2+ channels. Objective : The aim of the study was to assess the participation of B-type calcium channels in the alteration of membrane permeability to calcium ions consecutively to mutation of the d-sarcoglycan gene, in vascular smooth muscle cell (VSMC), in the cardiomyopathic Syrian hamster strain CHF 147. Methods : Single channels activity was recorded using the patch-clamp technique, in inside-out configurations, in normal and cardiomyopathic VSMC, and is reported in relative nPo Æ SE. Results : Typical voltage-independent B-type Ca2+ channel activity was detected in plasma membrane of freshly isolated and cultured VSMC, from either normal or cardiomyopathic hamster. In normal VSMC, activity was very low when freshly isolated (nPo : 0.024 Æ 0.011; n=34), significantly increased in non-proliferative culture (0.097 Æ 0.025, n=45) and was much higher in proliferative culture (0.15 Æ 0.06; n=41), but decreased with the increase in confluence. Interestingly in cardiomyopathic VSMC, in all cases, the channel activity was markedly higher, comparable to the reported chlorpromazine-induced activity in cardiomyocytes and was blocked by eosin (50 µM). Conclusion : These results show that B-type calcium channel activity is clearly modified in proliferative VSMC and in the model of cardiomyopathy underlying mutation of the d-sarcoglycan gene.
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