Role of atrial natriuretic peptide in pulmonary permeability and vasoregulation in ovine sepsis

Stubbe, Henning D.; Traber, Daniel L.; Booke, Michael; Traber, Lillian D.; Westphal, Martin; Aken, Hugo Van; Hinder, Frank

doi:10.1097/01.ccm.0000147834.01191.4e

Cited by 8 publications

(2 citation statements)

References 34 publications

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“…According to Hinder et al ( 1997 ) and Stubbe et al ( 2004 ) described that NPR-A/B antagonist preventing hypotension due to sepsis. This is the first mention that endogenous CNP or NPR-B intrinsic activity can contribute to modulation of vascular tone in aortas from Sham and CLP rats.…”

Section: Discussionmentioning

confidence: 99%

C-Type Natriuretic Peptide Induces Anti-contractile Effect Dependent on Nitric Oxide, Oxidative Stress, and NPR-B Activation in Sepsis

et al. 2016

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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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Section: Discussionmentioning

confidence: 99%

C-Type Natriuretic Peptide Induces Anti-contractile Effect Dependent on Nitric Oxide, Oxidative Stress, and NPR-B Activation in Sepsis

et al. 2016

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“…Furthermore, ANP and BNP concentrations in the circulation are increased in cardiovascular diseases such as heart failure, which is a common complication of sepsis (Potter et al, 2006). Indeed, in an experimental model of ovine sepsis, selective blockade of the natriuretic peptide receptor A and B (NPR-A/B) by HS-142-1 reverses many indices of myocardial depression associated with the condition (Hinder et al, 1997;Stubbe et al, 2004). Hence, it has been proposed that ANP and cyclic GMP (cGMP) (the intracellular second messenger responsible for mediating the biological activity of ANP) could be markers of severe and fatal myocardial depression early in the course of human endotoxic shock (Hartemink et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Resistance to endotoxic shock in mice lacking natriuretic peptide receptor‐A

et al. 2008

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Background and purpose: Excessive production of nitric oxide (NO) by inducible NO synthase (iNOS) is thought to underlie the vascular dysfunction, systemic hypotension and organ failure that characterize endotoxic shock. Plasma levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are raised in animal models and humans with endotoxic shock and correlate with the associated cardiovascular dysfunction. Since both NO and natriuretic peptides play important roles in cardiovascular homeostasis via activation of guanylate cyclase-linked receptors, we used mice lacking natriuretic peptide receptor (NPR)-A (NPR1) to establish if natriuretic peptides contribute to the cardiovascular dysfunction present in endotoxic shock. Experimental approach: Wild-type (WT) and NPR-A knockout (KO) mice were exposed to lipopolysaccharide (LPS) and vascular dysfunction (in vitro and in vivo), production of pro-inflammatory cytokines, and iNOS expression and activity were evaluated. Key results: LPS-treated WT animals exhibited a marked fall in mean arterial blood pressure (MABP) whereas NPR-A KO mice maintained MABP throughout. LPS administration caused a greater suppression of vascular responses to the thromboxanemimetic U46619, ANP, acetylcholine and the NO-donor spermine-NONOate in WT versus NPR-A KO mice. This differential effect on vascular function was paralleled by reduced pro-inflammatory cytokine production, iNOS expression and activity (plasma [NOx] and cyclic GMP). Conclusions and implications: These observations suggest that NPR-A activation by natriuretic peptides facilitates iNOS expression and contributes to the vascular dysfunction characteristic of endotoxic shock. Pharmacological interventions that target the natriuretic peptide system may represent a novel approach to treat this life-threatening condition.

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Possible contribution of the neprilysin/ACE pathway to sepsis in mice

Uğan

Gürbüz

et al. 2020

Life Sciences

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Role of atrial natriuretic peptide in pulmonary permeability and vasoregulation in ovine sepsis

Abstract: Blockade of atrial natriuretic peptide receptors increases pulmonary transvascular fluid flux independent of changes in permeability to protein in chronic ovine sepsis. Atrial natriuretic peptide may therefore play a protective role for the alveolar-capillary barrier during sepsis.

Cited by 8 publications

References 34 publications

C-Type Natriuretic Peptide Induces Anti-contractile Effect Dependent on Nitric Oxide, Oxidative Stress, and NPR-B Activation in Sepsis

C-Type Natriuretic Peptide Induces Anti-contractile Effect Dependent on Nitric Oxide, Oxidative Stress, and NPR-B Activation in Sepsis

Resistance to endotoxic shock in mice lacking natriuretic peptide receptor‐A

Possible contribution of the neprilysin/ACE pathway to sepsis in mice

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