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1 Division of Pediatric Cardiology, Mayo Clinic Rochester, Rochester, MN, USA
2 Department of Surgery, Mayo Clinic Rochester, Rochester, MN, USA
3 Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN, USA
4 Department of Surgery, Mayo Clinic Rochester, Rochester, MN, USA; Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: miller.virginia{at}mayo.edu.
Vascular function changes following loss of ovarian hormones in women at menopause and in experimental animals following surgical ovariectomy. Little is known about changes in vascular function during hormonal transition from sexual immaturity (juvenile) to sexual maturity. Therefore, experiments were designed to determine effects of natural puberty on vascular function in female pigs. Tissue was studied from 8 juvenile (2-3 months) and 8 adult (5-6 months) female pigs. Plasma nitric oxide (NO) was measured, and mRNA for endothelium-derived NO synthase (eNOS) and eNOS protein were determined in aortic endothelial cells. Rings of coronary arteries were suspended for measurement of isometric force in organ chambers. Serum 17
-estradiol levels were comparable in the two groups whereas the arithmetic mean of progesterone levels was about two-thirds lower in adults compared to juvenile pigs. Plasma NO was significantly higher in juveniles compared to adults but mRNA and protein for eNOS were comparable. In coronary arteries, an alpha2-adrenergic agonist caused greater endothelium-dependent relaxations in rings from juvenile compared to adult pigs. Relaxations to bradykinin were similar in arteries from both groups but inhibition of nitric oxide reduced relaxations only in arteries from juvenile pigs. Relaxations to NO were greater in arteries from adult compared to juvenile females. In conclusion, coronary arterial endothelial and smooth muscle responses are selectively modulated at puberty in female pigs. At maturity, plasma NO is reduced and sensitivity of the smooth muscle to exogenous NO is increased. Post-transcriptional regulation of eNOS protein may explain differences in NO bioavailability in juvenile pigs.
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