Colocalization of voltage-gated Na+ channels with the Na+/Ca2+ exchanger in rabbit cardiomyocytes during development.

Reverse-mode activity of the Na(+)/Ca(2+) exchanger (NCX) has been previously shown to play a prominent role in excitation-contraction coupling in the neonatal rabbit heart, where we have proposed that a restricted subsarcolemmal domain allows a Na(+) current to cause an elevation in the Na(+) concentration sufficiently large to bring Ca(2+) into the myocyte through reverse-mode NCX. In the present study, we tested the hypothesis that there is an overlapping expression and distribution of voltage-gated Na(+) (Na(v)) channel isoforms and the NCX in the neonatal heart. For this purpose, Western blot analysis, immunocytochemistry, confocal microscopy, and image analyses were used.

Distribution patterns of the Na+-Ca2+ exchanger and caveolin-3 in developing rabbit cardiomyocytes.

In adult cardiac cells the established mechanism of excitation-contraction coupling is by calcium-induced calcium release (CICR) mediated by L-type Ca(2+) channels. However, in neonate cardiomyocytes, a CICR modality involving reverse mode Na(+)-Ca(2+) exchanger (NCX) activity predominates. This has been hypothesized to be due, in part, to the high expression levels of NCX in the neonate heart which drop several fold during ontogeny.

Na+/H+ exchange inhibition with HOE 642 improves recovery of the injured neonatal rabbit heart.

Background: The effects of inhibition of the Na+/H+ exchanger (NHE) on postischemic recovery of the injured neonatal rabbit heart were examined. The NHE may be an important mechanism for reperfusion injury in the neonate heart. The effects of two NHE inhibitors, HOE 642 (HOE) and 5-(N,N-dimethyl)-amiloride (DMA), given during hypothermic cardioplegic arrest, were evaluated.