17 beta-Estradiol increases nitric oxide and prostaglandin I-2 production by cultured human uterine arteries only in histologically normal specimens

Citation
S. Obayashi et al., 17 beta-Estradiol increases nitric oxide and prostaglandin I-2 production by cultured human uterine arteries only in histologically normal specimens, J CARDIO PH, 38(2), 2001, pp. 240-249
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
0160-2446 → ACNP
Volume
38
Issue
2
Year of publication
2001
Pages
240 - 249
Database
ISI
SICI code
0160-2446(200108)38:2<240:1BINOA>2.0.ZU;2-D
Abstract
These experiments were designed to investigate whether 17 beta -estradiol ( E-2) modulates the endothelial function of perimenopausal human uterine art eries. After the artery specimen was cultured in the presence or absence of E-2 at a physiologic concentration of 200 pg/ml, changes in isometric tens ion and cyclic nucleotide production were determined. Degree of intimal hyp erplasia was assessed histologically and expressed as intima-to-media ratio . Acetylcholine produced an endothelium-dependent relaxation in six specime ns (group I) of 12, which was inhibited by N-G-nitro-L-arginine or indometh acin. However. the agonist failed to produce a definite relaxation in the r emaining 6 (group II) The endothelium-dependent relaxation was significantl y augmented after incubating with E-2 only in group I specimens. Cyclic nuc leotide production was significantly increased after E-2 incubation only in group I specimens, whereas it was inhibited by N-G-niho-L-arginine or indo methacin. Histologic study revealed that the six specimens of group I had n ormal intima (intima-to-media ratio = 19.1 +/-1.8%) and the remaining six o f group II had intimal hyperplasia (intima-to-media ratio = 53.6 +/-5.3%). Increased production of cyclic nucleotides occurred in uterine arteries wit h normal intima but not in arteries with intimal hyperplasia derived from p erimenopausal women.