Pernomian Laena, Prado Alejandro F, Silva Bruno R, Azevedo Aline, Pinheiro Lucas C, Tanus-Santos José E, Bendhack Lusiane M
Department of Pharmacology, School of Medicine of Ribeirão Preto (FMRP), University of São Paulo Ribeirão Preto, Brazil.
Department of Physics and Chemistry, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo Ribeirão Preto, Brazil.
Front Physiol. 2016 Jun 23;7:226. doi: 10.3389/fphys.2016.00226. eCollection 2016.
To evaluate the role of nitric oxide, reactive oxygen species (ROS), and natriuretic peptide receptor-B activation in C-type natriuretic peptide-anti-contractile effect on Phenylephrine-induced contraction in aorta isolated from septic rats.
Cecal ligation and puncture (CLP) surgery was used to induce sepsis in male rats. Vascular reactivity was conducted in rat aorta and resistance mesenteric artery (RMA). Measurement of survival rate, mean arterial pressure (MAP), plasma nitric oxide, specific protein expression, and localization were evaluated. Septic rats had a survival rate about 37% at 4 h after the surgery, and these rats presented hypotension compared to control-operated (Sham) rats. Phenylephrine-induced contraction was decreased in sepsis. C-type natriuretic peptide (CNP) induced anti-contractile effect in aortas. Plasma nitric oxide was increased in sepsis. Nitric oxide-synthase but not natriuretic peptide receptor-B expression was increased in septic rat aortas. C-type natriuretic peptide-anti-contractile effect was dependent on nitric oxide-synthase, ROS, and natriuretic peptide receptor-B activation. Natriuretic peptide receptor-C, protein kinase-Cα mRNA, and basal nicotinamide adenine dinucleotide phosphate (NADPH)-dependent ROS production were lower in septic rats. Phenylephrine and CNP enhanced ROS production. However, stimulated ROS production was low in sepsis.
CNP induced anti-contractile effect on Phenylephrine contraction in aortas from Sham and septic rats that was dependent on nitric oxide-synthase, ROS, and natriuretic peptide receptor-B activation.
评估一氧化氮、活性氧（ROS）和利钠肽受体-B激活在C型利钠肽对脓毒症大鼠离体主动脉中去氧肾上腺素诱导的收缩的抗收缩作用中的作用。
采用盲肠结扎穿刺（CLP）手术诱导雄性大鼠发生脓毒症。在大鼠主动脉和肠系膜阻力动脉（RMA）中进行血管反应性实验。评估存活率、平均动脉压（MAP）、血浆一氧化氮、特定蛋白表达和定位。脓毒症大鼠术后4小时存活率约为37%，与假手术（Sham）对照组大鼠相比，这些大鼠出现低血压。脓毒症时去氧肾上腺素诱导的收缩减弱。C型利钠肽（CNP）在主动脉中诱导抗收缩作用。脓毒症时血浆一氧化氮增加。脓毒症大鼠主动脉中一氧化氮合酶表达增加，但利钠肽受体-B表达未增加。C型利钠肽的抗收缩作用依赖于一氧化氮合酶、ROS和利钠肽受体-B激活。脓毒症大鼠中利钠肽受体-C、蛋白激酶-Cα mRNA和基础烟酰胺腺嘌呤二核苷酸磷酸（NADPH）依赖性ROS产生较低。去氧肾上腺素和CNP增强ROS产生。然而，脓毒症时刺激的ROS产生较低。
CNP对假手术组和脓毒症大鼠主动脉中去氧肾上腺素收缩具有抗收缩作用，该作用依赖于一氧化氮合酶、ROS和利钠肽受体-B激活。
