Placental protein 13 (PP13)-induced vasodilation of resistance arteries from pregnant and nonpregnant rats occurs via endothelial-signaling pathways. (3rd April 2017)

• Record Type: Journal Article
• Authors: Drobnjak, Tijana; Gizurarson, Sveinbjörn; Gokina, Natalia I.; Meiri, Hamutal; Mandalá, Maurizio; Huppertz, Berthold; Osol, George
• Is Part Of: Hypertension in pregnancy. Volume 36:Number 2(2017)
• Page Start: 186
• Page End: 195
• Publication Date: 2017-04-03
• Subjects: eNOS -- prostacyclin (PGI2) -- uterine vasculature -- endothelial layers -- preeclampsia; Hypertension in pregnancy -- Periodicals; Pregnancy -- Complications -- Periodicals; 618.3261
• DOI: 10.1080/10641955.2017.1295052
• Languages: English
• ISSNs: 1064-1955

Abstract

ABSTRACT: Placental protein 13 (PP13) induces hypotension in rats. This study aims to evaluate PP13 effects on isolated uterine arteries from nonpregnant and mid-pregnant rats. Vessels were isolated, cannulated, and pressurized to 50 mmHg within an arteriograph, preconstricted and exposed to increasing PP13 concentrations (10 −13 –10 −8 M). PP13 elicited 38–50% arterial vasodilation with half-maximum response (EC50 ) = 1 pM. The relaxation was mediated by activating the endothelial-signaling pathways of prostaglandin and nitric oxide (NO). Accordingly, these results encourage evaluation of PP13 as a possible therapy for gestational diseases characterized by insufficient uteroplacental blood flow and/or maternal hypertension.