In an embryonic chick model of persistent truncus arteriosus, L-type calcium currents are significantly reduced despite normal channel numbers, suggesting altered regulatory mechanisms akin to adult hearts under excessive hemodynamic burden.
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Suggests hemodynamic effects on embryonic calcium currents; hypothesis-generating and requires mammalian validation before any clinical relevance.
Calcium currents were examined in an experimental model in the embryonic chick heart with a congenital malformation known as persistent truncus arteriosus. This is a severe defect characterized by failure of conotruncal and aorticopulmonary septation of the embryonic heart tube. As a result, no separation into the aortic and pulmonary arteries occurs, and there is a common outflow tract. The hearts with persistent truncus arteriosus had a 26% greater ventricular to whole embryo weight, which indicated that the ventricles were enlarged. Both the low-threshold T-type (ICa.T) and the 1,4-dihydropyridine-sensitive L-type (ICa.L) Ca2+ currents were present in the ventricular myocytes from hearts at day 11 of incubation. However, day 11 hearts with persistent truncus arteriosus showed a twofold reduction in the peak magnitude of ICa.L at a test potential of + 10 mV without a concomitant reduction in the number of L channels detected by 1,4-dihydropyridine antagonist [(+)[3H]PN200-110] and agonist (Bay K 8644) receptor binding. The results indicated that an L channel regulatory mechanism other than protein synthesis was affected. These changes are consistent with responses to conditions of excessive hemodynamic burden that have been characterized in adult hearts.
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Tony L. Creazzo (1990) studied this question.
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