Chronic pressure overload is known to increase cardiac mass and expression levels of both
atrial natriuretic peptide (
ANP) and
brain natriuretic peptide (BNP) mRNAs. Although mechanical stretching of cardiac myocytes could cause these changes, humoral factor(s) secondary to pressure overload may also be involved. To dissociate humoral effects from the effects of mechanical loading on cardiac hypertrophic responses, we examined expression of
ANP and BNP at both
mRNA and
protein levels and proportions of
myosin isoforms in transplanted cervical hearts that were mechanically unloaded under conditions with or without
hypertension by
aortic coarctation. Seven days after
transplantation, cardiac atrophy that usually occurs in transplanted hearts without
hypertension by coarctation was prevented in the transplanted hearts with
hypertension by coarctation. The levels of expression of
ANP and BNP mRNAs were increased in the transplanted hearts with relative to those without
hypertension by coarctation. The plasma level of
angiotensin II was higher in rats with than without
hypertension by coarctation. Plasma
endothelin-1 levels were not significantly different between the two groups. In addition, levels of expression of
ANP and BNP mRNAs were increased in the transplanted hearts without
hypertension relative to those in the in situ hearts. The proportion of the V3
myosin isoform was also increased in the transplanted hearts without
hypertension relative to the in situ hearts. These results indicate that humoral factor(s) secondary to the pressure overload produced by
aortic coarctation enhanced the cardiac hypertrophic response and elevated the levels of mRNAs encoding these embryonic markers. Moreover, our findings regarding
ANP and BNP expression in the transplanted hearts provide additional evidence that the fetal genes are reexpressed during the process of cardiac
atrophy as well as in
cardiac hypertrophy.