title: Vascular responses to sodium nitroprusside in the human fetal-placental circulation.
abstract: This study examined the activity of sodium nitroprusside (SNP) in the human fetal-placental circulation in vitro in pathological and experimental conditions in which vascular function may be impaired. SNP (13-3400 nM) caused a concentration-dependent reduction in fetal arterial perfusion pressure (FAP) in Krebs' perfused placental cotyledons, at basal tone and following pre-constriction with prostaglandin F2 alpha (PGF2 alpha). SNP-induced reduction in FAP in the PGF2 alpha pre-constricted fetal-placental circulation was enhanced approximately six-fold (5.85) in those placentae pre-treated with the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (100 microM). Reductions in FAP in the preconstricted fetal-placental vasculature caused by SNP were not altered by prior infusion of ouabain (100 nM) into the fetal circulation or during low oxygen perfusion (O2 tension < 50 mmHg). No differences were observed in the responses obtained to SNP in placentae obtained from women with normotensive pregnancies or those associated with (i) pregnancy-induced hypertension, (ii) intra-uterine growth retardation, or (iii) an elevated umbilical-artery Doppler-ultrasound systolic/diastolic ratio, in either preconstricted placentae or those at basal tone. These findings are consistent with an up-regulation of guanylate cyclase/cGMP-mediated vasodilatation in the fetal-placental vasculature following complete blockade of endogenous NO production.
authors: Department of Obstetrics and Gynaecology, John Hunter Hospital, Newcastle, NSW, Australia.
authors: M A
authors: MA
authors: Read
authors: W B
authors: WB
authors: Giles
authors: I M
authors: IM
authors: Leitch
authors: A L
authors: AL
authors: Boura
authors: W A
authors: WA
authors: Walters
mesh_terms: D000293:Adolescent; D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D015237:Dinoprost / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology; D005333:Fetus / Q000098:blood supply* / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D066298:In Vitro Techniques; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine; D009599:Nitroprusside / Q000494:pharmacology*; D010042:Ouabain / Q000494:pharmacology; D010920:Placenta / Q000098:blood supply* / Q000187:drug effects; D011225:Pre-Eclampsia / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D009599:Nitroprusside; D019335:Nitroarginine; D010042:Ouabain; D001120:Arginine; D015237:Dinoprost; D019001:Nitric Oxide Synthase