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1Division of Pediatric Cardiology and Departments of 2Surgery and 3Physiology and Biophysics, Mayo Clinic Rochester, Rochester, Minnesota 55905
Submitted 8 April 2003 ; accepted in final form 1 May 2003
In humans, cardiovascular disease begins in young adulthood and is more
prevalent in males than females. However, little is known about vascular
function during transition to adulthood in males. The aim of this study was to
define changes in production of endothelium-derived nitric oxide (NO) and
coronary arterial responses during puberty. Plasma was collected from juvenile
(2–3 mo of age) and adult (5–6 mo of age) male pigs (n =
8/group) for measurement of NO, and aortic endothelial cells were collected
for measurement of mRNA and protein for endothelial NO synthase (eNOS).
Although plasma NO was higher in juvenile (67.0 ± 25.6 µM) than in
adult (15.0 ± 7.1 µM) male pigs, eNOS protein was similar in both
groups. However, levels of mRNA for eNOS were lower in aortic endothelial
cells from juvenile pigs. In rings of coronary arteries suspended in organ
chambers for measurement of isometric force and contracted with
PGF2
, relaxations to an
2-adrenergic agonist were significantly inhibited by
indomethacin only in juvenile pigs [EC50 (–log M), 6.7
± 0.3 with indomethacin and 7.7 ± 0.3 under control conditions].
NG-monomethyl-L-arginine (L-NMMA)
inhibited relaxations in both groups. On the contrary, in the presence of
indomethacin, relaxations to bradykinin were inhibited by L-NMMA
only in arteries from adult pigs [EC50 (–log M), 8.9 ±
0.3 with indomethacin and 8.6 ± 0.3 with addition of
L-NMMA]. These results suggest that hormonal changes associated
with sexual maturity may affect posttranscriptional and/or translational
regulation of eNOS protein and result in lower plasma NO in adult male pigs.
In addition, endothelium-derived inhibitory cyclooxygenase products seem to
predominate in juveniles.
cyclooxygenase; estrogen; testosterone; nitric oxide; prostacyclin
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