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1 Department of Internal Medicine, Cardiology Division, University of Texas Medical Branch, Galveston, Texas, USA
* To whom correspondence should be addressed. E-mail: mhuang1458{at}aol.com.
Intrinsic cardiac adrenergic (ICA) cells in the developing rat heart constitute a novel
adrenergic signaling system involved in cardiac regulation. The regulatory mechanisms
of ICA cells remain to be defined. Immunohistochemical study of fetal rat hearts
demonstrated ICA cells with catecholamine-biosynthetic enzyme tyrosine hydroxylase
(TH) and phenylethanolamine N-methyltransferase (PNMT). The mRNA of TH and
PNMP was also detected in fetal rat hearts before sympathetic innervation.
Immunoreactivity of norepinephrine transporter (NET) was localized to the ICA cells in
rat heart tissue and primary cell culture. For the functional study, the activity of [Ca2+]i
transients was quantified by a ratio fluorescent spectrometer in cultured ICA cells and
myocytes. ICA cells generated spontaneous [Ca2+]i transients that were eliminated by
tetrodotoxin or Ca2+-free solutions and showed greatly reduced amplitude with the
addition of L-type Ca2+ channel blocker nifedipine. [3H]norepinephrine studies
demonstrate release and uptake of norepinephrine. Functional interaction between
catecholamines produced by the ICA cells and cocultured myocytes was evident by the
effect of the 
-adrenergic blocker atenolol eliciting a dose-dependent reduction in the
amplitude and frequency of [Ca2+]i transients of beating myocytes. Hypoxia inhibited
[Ca2+]i transient activity of ICA cells which subsequently produced a reoxygenationmediated
rebound augmentation of [Ca2+]i transients. We conclude that ICA cells are
capable of catecholamine synthesis, release and uptake. They generate spontaneous
[Ca2+]i transient activity that can be regulated by oxygen tension. ICA cells may provide
an alternative adrenergic supply to maintain cardiac contractile and pacemaker function
at rest and during stress in the absence of sympathetic innervation.
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