Vasonatrin peptide stimulates both of the natriuretic peptide receptors, NPRA and NPRB

Jiang, Yebin; Lei, Jianyong; Chen, Y.; Jin, Jian

doi:10.1016/j.bbrc.2014.03.110

Cited by 6 publications

(3 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, ANP and BNP mainly bind to NPR-A, while CNP functions via NPR-B. A recent study has shown that cGMP stimulated by VNP in NPR-B-transfected cells was 11-fold higher than that of NPR-A (18). It seems that VNP binds preferentially to NPR-B and stimulates cGMP production.…”

Section: Discussionmentioning

confidence: 99%

Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms

Shi

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Diabetes mellitus increases morbidity/mortality of ischemic heart disease. Although atrial natriuretic peptide and C-type natriuretic peptide reduce the myocardial ischemia-reperfusion damage in nondiabetic rats, whether vasonatrin peptide (VNP), the artificial synthetic chimera of atrial natriuretic peptide and C-type natriuretic peptide, confers cardioprotective effects against ischemia-reperfusion injury, especially in diabetic patients, is still unclear. This study was designed to investigate the effects of VNP on ischemia-reperfusion injury in diabetic rats and to further elucidate its mechanisms. The high-fat diet-fed streptozotocin-induced diabetic Sprague-Dawley rats were subjected to ischemia-reperfusion operation. VNP treatment (100 μg/kg iv, 10 min before reperfusion) significantly improved the instantaneous first derivation of left ventricle pressure (±LV dP/dtmax) and LV systolic pressure and reduced LV end-diastolic pressure, apoptosis index, caspase-3 activity, plasma creatine kinase (CK), and lactate dehydrogenase (LDH) activities. Moreover, VNP inhibited endoplasmic reticulum (ER) stress by suppressing glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP). These effects were mimicked by 8-bromine-cyclic guanosinemonophosphate (8-Br-cGMP), a cGMP analog, whereas they were inhibited by KT-5823, the selective inhibitor of PKG. In addition, pretreatment with tauroursodeoxycholic acid (TUDCA), a specific inhibitor of ER stress, could not further promote the VNP's cardioprotective effect in diabetic rats. In vitro H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation and incubated with or without VNP (10(-8) mol/l). Gene knockdown of PKG1α with siRNA blunted VNP inhibition of ER stress and apoptosis, while overexpression of PKG1α resulted in significant decreased ER stress and apoptosis. VNP protects the diabetic heart against ischemia-reperfusion injury by inhibiting ER stress via the cGMP-PKG signaling pathway. These results suggest that VNP may have potential therapeutic value for the diabetic patients with ischemic heart disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms

Shi

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Vasonatrin (VNP) is a synthetic peptide consisting of the full-length 22-amino acid CNP and the 5-AA C-terminus of ANP (Wei et al, 1993b). It has been shown to stimulate both NPR-A and -B (Jiang et al, 2014) and to be a more potent vasorelaxant than ANP (Wei et al, 1993b). In an animal model of ischemic cardiomyopathy, infusion of VNP was shown to improve hemodynamic parameters through a cGMP/PKG-dependent mechanism (Shi et al, 2015).…”

Section: Designer Npsmentioning

confidence: 99%

Toward a New Paradigm for Targeted Natriuretic Peptide Enhancement in Heart Failure

Gidlöf

2021

Front. Physiol.

View full text Add to dashboard Cite

The natriuretic peptide system (NPS) plays a fundamental role in maintaining cardiorenal homeostasis, and its potent filling pressure-regulated diuretic and vasodilatory effects constitute a beneficial compensatory mechanism in heart failure (HF). Leveraging the NPS for therapeutic benefit in HF has been the subject of intense investigation during the last three decades and has ultimately reached widespread clinical use in the form of angiotensin receptor-neprilysin inhibition (ARNi). NPS enhancement via ARNi confers beneficial effects on mortality and hospitalization in HF, but inhibition of neprilysin leads to the accumulation of a number of other vasoactive peptides in the circulation, often resulting in hypotension and raising potential concerns over long-term adverse effects. Moreover, ARNi is less effective in the large group of HF patients with preserved ejection fraction. Alternative approaches for therapeutic augmentation of the NPS with increased specificity and efficacy are therefore warranted, and are now becoming feasible particularly with recent development of RNA therapeutics. In this review, the current state-of-the-art in terms of experimental and clinical strategies for NPS augmentation and their implementation will be reviewed and discussed.

show abstract

“…In this way the clinical use of synthesized analogs of natriuretic peptides such as anaritide, vasonatrin, ularitide, and nesiritide must be considered in the future [85–87]. Furthermore, pharmacological agents with dual action (inhibitor/enhancer) on the renin-angiotensin and natriuretic peptide systems like omapatrilat have been used successfully in clinical trials for hypertension treatment [88, 89].…”

Section: Future Perspectivesmentioning

confidence: 99%

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

Choi

Mikusic

Kouyoumdzian

et al. 2014

BioMed Research International

View full text Add to dashboard Cite

Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.

show abstract

Vasonatrin peptide stimulates both of the natriuretic peptide receptors, NPRA and NPRB

Cited by 6 publications

References 19 publications

Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms

Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms

Toward a New Paradigm for Targeted Natriuretic Peptide Enhancement in Heart Failure

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

Contact Info

Product

Resources

About