Signaling cascade that mediates endothelial nitric oxide synthase activation induced by atrial natriuretic peptide

Elesgaray, Rosana; Caniffi, Carolina; Ierace, Daniela Rodríguez; Jaime, María Florencia Visintini; Fellet, Andrea L.; Arranz, Cristina; Costa, María A.

doi:10.1016/j.regpep.2008.05.008

Cited by 30 publications

(28 citation statements)

References 29 publications

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“…Furthermore, we have reported that the NPR-C natriuretic receptor mediates activation of NOS by ANP in the kidney (4,11). In contrast, McLay et al (22) have shown that, in cultures of proximal tubular cells, ANP inhibits iNOS activity via NPR-C and cGMP.…”

mentioning

confidence: 92%

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Elesgaray

Caniffi

Savignano

et al. 2012

American Journal of Physiology-Renal Physiology

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Atrial natriuretic peptide (ANP) is an important regulator of blood pressure (BP). One of the mechanisms whereby ANP impacts BP is by stimulation of nitric oxide (NO) production in different tissues involved in BP control. We hypothesized that ANP-stimulated NO is impaired in the kidneys of spontaneously hypertensive rats (SHR) and this contributes to the development and/or maintenance of high levels of BP. We investigated the effects of ANP on the NO system in SHR, studying the changes in renal nitric oxide synthase (NOS) activity and expression in response to peptide infusion, the signaling pathways implicated in the signaling cascade that activates NOS, and identifying the natriuretic peptide receptors (NPR), guanylyl cyclase receptors (NPR-A and NPR-B) and/or NPR-C, and NOS isoforms involved. In vivo, SHR and Wistar-Kyoto rats (WKY) were infused with saline (0.05 ml/min) or ANP (0.2 μg·kg(-1)·min(-1)). NOS activity and endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) NOS expression were measured in the renal cortex and medulla. In vitro, ANP-induced renal NOS activity was determined in the presence of iNOS and nNOS inhibitors, NPR-A/B blockers, guanine nucleotide-regulatory (G(i)) protein, and calmodulin inhibitors. Renal NOS activity was higher in SHR than in WKY. ANP increased NOS activity, but activation was lower in SHR than in WKY. ANP had no effect on expression of NOS isoforms. ANP-induced NOS activity was not modified by iNOS and nNOS inhibitors. NPR-A/B blockade blunted NOS stimulation via ANP in kidney. The renal NOS response to ANP was reduced by G(i) protein and calmodulin inhibitors. We conclude that ANP interacts with NPR-C, activating Ca-calmodulin eNOS through G(i) protein. NOS activation also involves NPR-A/B. The NOS response to ANP was diminished in kidneys of SHR. The impaired NO system response to ANP in SHR participates in the maintenance of high blood pressure.

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mentioning

confidence: 92%

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Elesgaray

Caniffi

Savignano

et al. 2012

American Journal of Physiology-Renal Physiology

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“…In contrast, cGMP/ PKG pathway appeared to have a role in NOS activity stimulated by ANP in aorta, left ventricle and kidney. In fact, ANP-induced increase of NOS activity was abolished by a calmodulin antagonist in all tissues, implying a Ca 2þ -calmodulin-dependent NOS pathway [76].…”

Section: Atrial Natriuretic Peptide and Nitric Oxide Systemmentioning

confidence: 85%

“…Elesgaray et al [76] evaluated the NOS isoform involved in the ANP effects, the changes in NOS expression and the related signaling pathways. NOS activity induced by ANP was not modified under either iNOS or nNOS inhibitors in aorta, heart and kidney, suggesting that eNOS is the isoform involved.…”

Section: Atrial Natriuretic Peptide and Nitric Oxide Systemmentioning

confidence: 99%

Atrial natriuretic peptide and regulation of vascular function in hypertension and heart failure

Rubattu¹,

Calvieri²,

Pagliaro³

et al. 2013

Journal of Hypertension

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Atrial natriuretic peptide (ANP) plays a pivotal role in modulation of vascular function and it is also involved in the pathophysiology of several cardiovascular diseases. We provide an updated overview of the current appraisal of ANP vascular effects in both animal models and humans. We describe the physiological implications of ANP vasomodulatory properties as well as the involvement of ANP, through its control of vascular function, in hypertension and heart failure. The principal molecular mechanisms underlying regulation of vascular tone, that is natriuretic peptide receptor type A/cyclic guanylate monophosphate, natriuretic peptide receptor type C, nitric oxide system, are discussed. We review the literature on therapeutic implications of ANP in hypertension and heart failure, examining the potential use of ANP analogues, neutral endopeptidase (NEP) inhibitors, ACE/NEP inhibitors, angiotensin receptor blocker (ARB)/NEP inhibitors, the new dual endothelin-converting enzyme (ECE)/NEP inhibitors and ANP-based gene therapy. The data discussed support the role of ANP in different pathological conditions through its vasomodulatory properties. They also indicate that ANP may represent an optimal therapeutic agent in cardiovascular diseases.

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“…Tissue slices (2-3 mm thick) from Eut, hypo and hyper animals were obtained. Some slices from haemorrhaged groups were pre-incubated (15 min) with calmidazolium (Cz, 1 µM) (Elesgaray et al 2008) before incubation with [ 14 C (U)] l-arginine during 30 min at 37°C. The amount of [ 14 C] l-citrulline obtained was determined with a liquid scintillation counter.…”

Section: Calcium Dependencementioning

confidence: 99%

Thyroid disorders and nitric oxide in cardiovascular adaptation to hypovolemia

Ogonowski

Piro

Pessah

et al. 2016

Journal of Endocrinology

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This study aimed to investigate whether nitric oxide participates in the cardiovascular function and haemodynamic adaptation to acute haemorrhage in animals with thyroid disorders. Sprague-Dawley rats aged 2months old treated with T3 (hyper, 20μg/100g body weight) or 0.02% methimazole (hypo, w/v) during 28days were pre-treated with NG nitro-l-arginine methyl ester (L-NAME) and submitted to 20% blood loss. Heart function was evaluated by echocardiography. Measurements of arterial blood pressure, heart rate, nitric oxide synthase activity and protein levels were performed. We found that hypo decreased fractional shortening and ejection fraction and increased left ventricle internal diameter. Hyper decreased ventricle diameter and no changes in cardiac contractility. Haemorrhage elicited a hypotension of similar magnitude within 10min. Then, this parameter was stabilized at about 30–40min and maintained until finalized, 120min. L-NAME rats showed that the immediate hypotension would be independent of nitric oxide. Nitric oxide synthase inhibition blunted the changes of heart rate induced by blood loss. Hyper and hypo had lower atrial enzyme activity associated with a decreased enzyme isoform in hypo. In ventricle, hyper and hypo had a higher enzyme activity, which was not correlated with changes in protein levels. Haemorrhage induced an increased heart nitric oxide production. We concluded that thyroid disorders were associated with hypertrophic remodelling which impacted differently on cardiac function and its adaptation to a hypovolemia. Hypovolemia triggered a nitric oxide synthase activation modulating the heart function to maintain haemodynamic homeostasis. This involvement depends on a specific enzyme isoform, cardiac chamber and thyroid state.

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Signaling cascade that mediates endothelial nitric oxide synthase activation induced by atrial natriuretic peptide

Cited by 30 publications

References 29 publications

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Atrial natriuretic peptide and regulation of vascular function in hypertension and heart failure

Thyroid disorders and nitric oxide in cardiovascular adaptation to hypovolemia

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