title: Investigation of the role of the NO-cGMP pathway on YC-1 and DEA/NO effects on thoracic aorta smooth muscle responses in a rat preeclampsia model.
abstract: The present study was designed to investigate the effects of YC-1, a nitric oxide (NO)-independent soluble guanylate cyclase (sGC) activator, and DEA/NO, a NO donor, on smooth muscle responses in the preeclampsia model with suramin-treated rats and on the levels of cyclic guanosine monophosphate (cGMP) of thoracic aorta rings isolated from term-pregnant rats. Rats of 2 groups, control group and suramin group, were given intraperitoneal injection of saline or suramin, respectively. Suramin injection caused increased blood pressure, protein in urine, and fetal growth retardation. Thoracic aorta rings were exposed to contractile and relaxant agents. KCl contraction and papaverine relaxation responses were similar. Relaxation responses of YC-1 and DEA/NO decreased in suramin group. In both groups in the presence of ODQ, a sGC inhibitor, the relaxation responses of YC-1 and DEA/NO decreased. The cGMP content was determined by radioimmunoassay technique. The content of cGMP in the suramin group decreased. In the presence of YC-1 and DEA/NO in both groups, cGMP content increased, but in ODQ-added groups, there was a significant decrease. We conclude that in preeclampsia, the decrease of relaxation responses and the decrease of cGMP content could be due to the reduction in stimulation of sGC and the decrease in cGMP levels.
authors.affiliation: a Department of Pharmacology, Faculty of Pharmacy, Cumhuriyet University, Sivas 58140, Turkey.
authors.forename: Nergiz Hacer
authors.initials: NH
authors.lastname: Turgut
authors.forename: Tijen Kaya
authors.initials: TK
authors.lastname: Temiz
authors.forename: Bülent
authors.initials: B
authors.lastname: Turgut
authors.forename: Baris
authors.initials: B
authors.lastname: Karadas
authors.forename: Mesut
authors.initials: M
authors.lastname: Parlak
authors.forename: Ihsan
authors.initials: I
authors.lastname: Bagcivan
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation; D020536:Enzyme Activators / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000378:metabolism; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors / Q000378:metabolism; D007191:Indazoles / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology*; D011225:Pre-Eclampsia / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D011507:Proteinuria / Q000139:chemically induced / Q000378:metabolism; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D015290:Second Messenger Systems / Q000187:drug effects; D013498:Suramin; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D020536:Enzyme Activators; D004791:Enzyme Inhibitors; D007191:Indazoles; D020030:Nitric Oxide Donors; D000644:Quaternary Ammonium Compounds; D014665:Vasodilator Agents; C406802:diethylammonium-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate; C090937:3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole; D009569:Nitric Oxide; D013498:Suramin; D006162:Guanylate Cyclase; D006152:Cyclic GMP