GESTATION INCREASES NITRIC OXIDE-MEDIATED VASODILATION IN RAT UTERINEARTERIES

Authors
Citation
Yj. Ni et al., GESTATION INCREASES NITRIC OXIDE-MEDIATED VASODILATION IN RAT UTERINEARTERIES, American journal of obstetrics and gynecology, 176(4), 1997, pp. 856-864
Citations number
22
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00029378
Volume
176
Issue
4
Year of publication
1997
Pages
856 - 864
Database
ISI
SICI code
0002-9378(1997)176:4<856:GINOVI>2.0.ZU;2-T
Abstract
OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reacti vity during pregnancy. STUDY DESIGN: The effects of pregnancy on endot helial function were evaluated in isolated pressurized rat uterine art eries from late-pregnant rats (day 19 to 20) versus age-matched nonpre gnant controls. The effects of nitric oxide synthase inhibition (N-ome ga-nitro-L-arginine) on arterial tone and reactivity under basal and a ctivated (phenylephrine) conditions were determined, as was arterial r eactivity to endothelium-dependent (acetylcholine) and endothelium-ind ependent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter. RESULTS: (1) Maximal constriction to N-omega-nitro-L- arginine was significantly enhanced under basal (nonstimulated) condit ions in arteries from late-pregnant versus nonpregnant rats (changes i n lumen diameter 37% +/- 8% vs 9.3 +/- 6.2%, respectively, p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L N-omega-nitro-L-argin ine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 +/- 23 nmol /L vs 33 +/- 8 nmol/L control vs treated vessels, p < 0.05) but was wi thout statistically significant effect on arteries from nonpregnant an imals (control 255 +/- 164 nmol/L, treated 250 +/- 102 nmol/L, p > 0.0 5). (3) The threshold concentration of acetytcholine required to elici t endothelium-dependent dilation was significantly lower in late-pregn ant versus nonpregnant arteries (1.4 +/- 0.2 nmol/L vs 12.2 +/- 3.8 nm ol/L, p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenou s nitrodilator (sodium nitroprusside) was identical in fate-pregnant v ersus nonpregnant vessels. CONCLUSION: Endothelial vasodilator influen ces are augmented during pregnancy under basal, activated (phenylephri ne), and chemically provoked (acetylcholine) conditions in uterine art eries by enhanced release of nitric oxide.