scholarly journals Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease

2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Emilie Balk-Møller ◽  
Johanne Agerlin Windeløv ◽  
Berit Svendsen ◽  
Jenna Hunt ◽  
Seyed Mojtaba Ghiasi ◽  
...  
Keyword(s):  
Lung Function ◽  
Mouse Model ◽  
Atrial Natriuretic Peptide ◽  
Lung Disease ◽  
Pulmonary Disease ◽  
Natriuretic Peptide ◽  
Obstructive Pulmonary Disease ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Atrial Natriuretic

Abstract Glucagon-like peptide-1 (GLP-1) is protective in lung disease models but the underlying mechanisms remain elusive. Because the hormone atrial natriuretic peptide (ANP) also has beneficial effects in lung disease, we hypothesized that GLP-1 effects may be mediated by ANP expression. To study this putative link, we used a mouse model of chronic obstructive pulmonary disease (COPD) and assessed lung function by unrestrained whole-body plethysmography. In 1 study, we investigated the role of endogenous GLP-1 by genetic GLP-1 receptor (GLP-1R) knockout (KO) and pharmaceutical blockade of the GLP-1R with the antagonist exendin-9 to -39 (EX-9). In another study the effects of exogenous GLP-1 were assessed. Lastly, we investigated the bronchodilatory properties of ANP and a GLP-1R agonist on isolated bronchial sections from healthy and COPD mice. Lung function did not differ between mice receiving phosphate-buffered saline (PBS) and EX-9 or between GLP-1R KO mice and their wild-type littermates. The COPD mice receiving GLP-1R agonist improved pulmonary function (P < .01) with less inflammation, but no less emphysema compared to PBS-treated mice. Compared with the PBS-treated mice, treatment with GLP-1 agonist increased ANP (nppa) gene expression by 10-fold (P < .01) and decreased endothelin-1 (P < .01), a peptide associated with bronchoconstriction. ANP had moderate bronchodilatory effects in isolated bronchial sections and GLP-1R agonist also showed bronchodilatory properties but less than ANP. Responses to both peptides were significantly increased in COPD mice (P < .05, P < .01). Taken together, our study suggests a link between GLP-1 and ANP in COPD.

Elevated levels of brain natriuretic peptide in acute hypoxaemic chronic obstructive pulmonary disease

1992 ◽  
Vol 83 (5) ◽  
pp. 529-533 ◽  
Author(s):  
Chim C. Lang ◽  
Wendy J. Coutie ◽  
Allan D. Struthers ◽  
D. Paul Dhillon ◽  
John H. Winter ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Pulmonary Disease ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Partial Pressure ◽  
Atrial Natriuretic

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 ± 0.4 kPa; arterial partial pressure of CO2, 6.9 ± 0.1 kPa; forced expiratory volume in 1 s, 0.6 ± 0.07 litre (27 ± 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 ± 4.1 pmol/l and 45.0 ± 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 ± 0.8 pmol/l and 8.0 ± 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = −0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide. 4. Thus, plasma levels of brain natriuretic peptide were proportionately higher than those of atrial natriuretic peptide in patients with hypoxaemic chronic obstructive pulmonary disease. Unlike those of atrial natriuretic peptide, plasma levels of brain natriuretic peptide were correlated with the degree of hypoxaemia. Further studies are required to investigate the release and clearance of brain natriuretic peptide in chronic obstructive pulmonary disease, as well as its pulmonary vasodilator activity in vivo.

scholarly journals Glucagon-like peptide-1: effect on pro-atrial natriuretic peptide in healthy males

2014 ◽  
Vol 3 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Jeppe Skov ◽  
Jens Juul Holst ◽  
Jens Peter Gøtze ◽  
Jørgen Frøkiær ◽  
Jens Sandahl Christiansen
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Young Males ◽  
Randomized Controlled ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Double Blinded ◽  
Atrial Natriuretic

The antihypertensive actions of glucagon-like peptide-1 (GLP1) receptor agonists have been linked to the release of atrial natriuretic peptide (ANP) in mice. Whether a GLP1–ANP axis exists in humans is unknown. In this study, we examined 12 healthy young males in a randomized, controlled, double-blinded, single-day, cross-over study to evaluate the effects of a 2-h native GLP1 infusion. Plasma proANP concentrations were measured by an automated mid-region-directed proANP immunoassay and N-terminal pro B-type natriuretic peptide (BNP) on Roche Modular E170. Urine was collected for measurements of sodium excretion. Although GLP1 infusion increased the urinary sodium excretion markedly, there were no significant changes in either proANP or proBNP concentrations. When GLP1 infusion was stopped, sodium excretion declined rapidly. As proANP concentration reflects ANP secretion, our data could not confirm the existence of a GLP1–ANP axis in humans. Especially, the natriuretic effects of GLP1 seem unlikely to be mediated exclusively via ANP.

Sign in / Sign up

Export Citation Format

Share Document