Key result
C-type natriuretic peptide induced an anti-contractile effect on phenylephrine contraction in aortas from sham and septic rats that was dependent on nitric oxide-synthase, reactive oxygen species, and natriuretic peptide receptor-B activation.
Why the study?
Does C-type natriuretic peptide induce an anti-contractile effect in aortas from septic rats?
Does C-type natriuretic peptide induce an anti-contractile effect in aortas from septic rats?
CNP induces an anti-contractile effect in sepsis that depends on NOS, ROS, and NPR-B activation, highlighting a potential mechanism for vascular hyporesponsiveness in septic shock.
CNP pathway effects in septic vessels merit targeted validation; leaves open any role in human sepsis.
AIMS: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.
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Pernomian et al. (2016) studied Sepsis (n=50). C-type natriuretic peptide (CNP) vs. Absence of CNP / Sham was evaluated on Phenylephrine-induced contraction in isolated aorta. C-type natriuretic peptide induced an anti-contractile effect on phenylephrine contraction in aortas from sham and septic rats that was dependent on nitric oxide-synthase, reactive oxygen species, and natriuretic peptide receptor-B activation.
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