scholarly journals An impaired natriuretic peptide hormone system may play a role in COVID‐19 severity in vulnerable populations

2020 ◽  
Vol 2 (10) ◽  
pp. 596-599
Author(s):  
Mark G. Currie ◽  
Daniel P. Zimmer ◽  
Perry V. Halushka
2020 ◽  
Author(s):  
Mark G. Currie ◽  
Daniel Zimmer ◽  
Perry Halushka

Advanced age, underlying cardiovascular disease (including hypertension), and obesity are associated with a higher risk of progression to severe hypoxemia, acute respiratory distress syndrome (ARDS), and death in COVID-19-infected patients. African Americans have a higher degree of COVID-19 mortality. The incidence of salt-sensitive hypertension is higher in older individuals and African Americans. Lower circulating levels of natriuretic peptides, key regulators of vascular tone and kidney function, have been associated with salt-sensitive hypertension and obesity. Evidence has accumulated that ANP administered to pulmonary endothelial cells, isolated lungs, and patients suffering from ARDS reduces endothelial damage and preserves the endothelial barrier, thereby reducing pulmonary edema and inflammation. Epidemiologic and pharmacologic data suggest that deficiencies in the natriuretic peptide hormone system may contribute to the development of severe lung pathology in COVID-19 patients, and treatments that augment natriuretic peptide signaling may have potential to limit progression to ARDS.


Bone ◽  
2008 ◽  
Vol 42 ◽  
pp. S80
Author(s):  
Grahame McKenzie ◽  
Bryn Hardwick ◽  
Blanca SanMiguel ◽  
Bik Chopra ◽  
Giovanna Creasey ◽  
...  

2007 ◽  
Vol 179 (3) ◽  
pp. 371-373 ◽  
Author(s):  
Christopher C. Glembotski

A study by Rybkin et al. (see p. 527) substantially advances our understanding of regulated exocytois by specialized secretory cells, such as atrial myocytes. A second member of the Ras-related protein family, RRP17, was identified and shown to participate in regulating the secretion of the cardiac-derived peptide hormone, atrial natriuretic peptide. In addition to the heart, RRP17 was shown to be expressed in neuronal, pancreatic, and skeletal muscle cells, suggesting a widespread role in regulated secretion for this new protein.


2001 ◽  
Vol 24 (7) ◽  
pp. RC22-RC24 ◽  
Author(s):  
Branka Mazul-Sunko ◽  
N. Zarkovic ◽  
N. Vrkic ◽  
R. Klinger ◽  
M. Peric ◽  
...  

2009 ◽  
Vol 297 (2) ◽  
pp. H550-H555 ◽  
Author(s):  
Gregori Casals ◽  
Josefa Ros ◽  
Alessandro Sionis ◽  
Mercy M. Davidson ◽  
Manuel Morales-Ruiz ◽  
...  

B-type natriuretic peptide (BNP) is a peptide hormone of myocardial origin with significant cardioprotective properties. Patients with myocardial ischemia present with high levels of BNP in plasma and elevated expression in the myocardium. However, the molecular mechanisms of BNP induction in the ischemic myocardium are not well understood. The aim of the investigation was to assess whether myocardial hypoxia induces the production of BNP in human ventricular myocytes. To test the hypothesis that reduced oxygen tension can directly stimulate BNP gene expression and release in the absence of hemodynamic or neurohormonal stimuli, we used an in vitro model system of cultured human ventricular myocytes (AC16 cells). Cells were cultured under normoxic (21% O2) or hypoxic (5% O2) conditions for up to 48 h. The accumulation of BNP, atrial natriuretic peptide (ANP), and vascular endothelial growth factor (VEGF) was then measured. Hypoxia stimulated the protein release of BNP and VEGF but not ANP. In concordance, the increased mRNA levels of BNP and VEGF but not ANP were found on culturing AC16 cells under hypoxic conditions. The analysis of the transcriptional activity of the hypoxia-inducible factor 1 (HIF-1) in nuclear extracts showed that HIF-1 activity was induced under hypoxic conditions. Finally, the treatment of AC16 cells with the HIF-1 inhibitor rotenone in hypoxia inhibited BNP and VEGF release. In conclusion, these data indicate that hypoxia induces the synthesis and secretion of BNP in human ventricular myocytes, likely through HIF-1-enhanced transcriptional activity.


2009 ◽  
Vol 55 (5) ◽  
pp. 878-887 ◽  
Author(s):  
Cristina Vassalle ◽  
Maria Grazia Andreassi

Abstract Background: The natriuretic peptide hormone family includes various proteins characterized by similar chemical structure and shared biological functions, with important effects on the cardiovascular system. Accordingly, these molecules are widely recognized as key clinical biomarkers in the diagnosis and monitoring of heart failure, hypertension, and coronary heart disease. Content: Several single-nucleotide polymorphisms have been recently identified in genes associated with the natriuretic system. This review provides an overview of new insights into the functional role of these genetic variants, as well as their impact on cardiovascular physiopathology and drug response. Conclusions: Noteworthy relationships between some specific polymorphisms and clinical correlates of cardiovascular disease have emerged. Nevertheless, future confirming studies are needed to substantiate the clinical relevance of such variants.


Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5313-5321 ◽  
Author(s):  
Michael Bensimon ◽  
Astra I. Chang ◽  
Mercedes L. Kuroski de Bold ◽  
Amalia Ponce ◽  
Daniel Carreras ◽  
...  

2010 ◽  
Vol 29 (1) ◽  
pp. 5-12
Author(s):  
Vladana Milisavljevic ◽  
Isabell Purdy ◽  
Cindy Le

This article reports a case of pulmonary hypertension in 37-week–gestational-age, pygopagus conjoined twins where B-type natriuretic peptide (BNP) was used as a cost-effective and important tool to aid effective management. Pulmonary hypertension in neonates is associated with high morbidity and mortality and multiplies the challenge of caring for conjoined twins. BNP is a peptide hormone secreted by cardiac ventricles that have undergone stress related to ventricular filling, volume overload, and pressure. BNP is commonly used in adults to assess heart failure, but its utility is less established in infants receiving neonatal intensive care. In this case, BNP testing was used as an adjunct to standard assessments for rapid diagnosis which was critical to expediting appropriate treatment management for these high-risk patients.


2019 ◽  
Vol 20 (24) ◽  
pp. 6128 ◽  
Author(s):  
In-Seon Bae ◽  
Sang Hoon Kim

The browning of white adipose tissue (beige adipocytes) stimulates energy expenditure. Omega-3 fatty acids have been shown to induce thermogenic action in adipocytes via G-protein coupled receptor 120 (GPR120). Atrial natriuretic peptide (ANP) is a peptide hormone that plays the role of maintaining normal blood pressure in kidneys to inhibit Na+ reuptake. Recently, ANP was found to induce adipocyte browning by binding to NPR1, an ANP receptor. However, the expression of ANP in adipocytes has not yet been studied. Therefore, in this study, we investigate the expression of ANP in beige-like adipocytes induced by docosahexaenoic acids (DHA), T3, or a PPAR agonist, rosiglitazone. First, we found that brown adipocyte-specific genes were upregulated in beige-like adipocytes. DHA promoted ANP expression in beige-like cells, whereas DHA-induced ANP expression was abolished by GPR120 knockout. ANP secretion of beige-like adipocytes was increased via PKC/ERK1/2 signaling in the GPR120 pathway. Furthermore, ANP secreted from beige-like adipocytes acted on HEK-293 cells, the recipient cells, leading to increased cGMP activity. After the NPR1 knockdown of HEK-293 cells, cGMP activity was not changed. Taken together, our findings indicate that beige-like adipocytes induce ANP secretion, which may contribute to improving obesity-associated metabolic disease.


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