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.

Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders

1987 ◽  
Vol 252 (5) ◽  
pp. F865-F871 ◽  
Author(s):  
J. P. Koepke ◽  
G. F. DiBona
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Atrial Natriuretic

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.

Atrial natriuretic peptide – cyclic GMP coupling and urinary sodium excretion during acute volume expansion in man

1990 ◽  
Vol 68 (4) ◽  
pp. 535-538 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Graham A. MacGregor ◽  
David G. Shirley ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Gmp ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Atrial Natriuretic

The present study examines hormonal and renal responses to acute volume expansion in normal man, with particular emphasis on the atrial natriuretic peptide (ANP) – cyclic GMP coupling. Two liters of isotonic saline were infused into eight normotensive male subjects over a 1-h period. Plasma and urinary measurements were made before, during, and up to 300 min after the start of the saline infusion. With the initial increase in urinary sodium excretion there were increases in plasma ANP and plasma cyclic GMP, which reached maximum levels at 15 min after the end of the saline infusion. Urinary cyclic GMP increased gradually during saline infusion up to approximately 60 min after the end of the infusion. Plasma ANP and plasma and urinary cyclic GMP excretion gradually declined thereafter. By contrast, urinary sodium excretion remained elevated up to the end of the observation period. The saline infusion was associated with marked reductions in plasma renin activity and aldosterone, which persisted up to the end of the study. These results suggest a coupling between the increases in plasma ANP, the production of cyclic GMP, and urinary sodium excretion, in particular during the initial renal response to acute volume expansion. However, other mechanisms including the suppression of the rennin–angiotensin–aldosterone system may become increasingly important in the later natriuretic response to acute volume expansion.Key words: atrial natriuretic peptide, cyclic GMP, sodium, renal, human.

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.

Atrial natriuretic peptide: Physiological release associated with natriuresis during water immersion in man

1986 ◽  
Vol 71 (3) ◽  
pp. 319-322 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Millar ◽  
J. P. O'Hare ◽  
J. C. MacKenzie ◽  
R. J. M. Corrall ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Natriuretic Hormone ◽  
The Mean ◽  
Atrial Natriuretic

1. Thermoneutral water immersion produces a physiological increase of thoracic blood volume, raises central venous pressure and increases urinary sodium excretion by a hitherto ill-understood mechanism. We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). 2. During water immersion there was a highly significant (P < 0.001) twofold increase of the mean plasma ANP concentration and a doubling of the mean urinary sodium excretion. Both were unchanged during the control experiments. 3. These results are consistent with the hypotheses (a) that ANP is released into plasma in response to central blood volume expansion and (b) that it functions as a natriuretic hormone in normal man under physiological conditions.

Dissociation between plasma atrial natriuretic peptide levels and urinary sodium excretion after intravenous saline infusion in normal man

1987 ◽  
Vol 73 (3) ◽  
pp. 285-289 ◽  
Author(s):  
Donald R. J. Singer ◽  
Angela C. Shore ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Giuseppe A. Sagnella ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Sodium Balance ◽  
Normal Male ◽  
Maximal Rise ◽  
Atrial Natriuretic

1. Plasma immunoreactive atrial natriuretic peptide (ANP) and urinary sodium excretion were measured in six normal male subjects before, during and for 195 min after a 60 min infusion of 2 litres of saline (0.9% NaCl, 308 mmol of Na+). 2. During the saline infusion, there was a significant increase in plasma ANP and urinary sodium excretion and a significant decrease in plasma renin activity, aldosterone, albumin, creatinine and packed cell volume. 3. The maximal rise in mean plasma ANP occurred 15 min after stopping the infusion and the maximal rise in mean urinary sodium excretion in the collection period 30 min later. 4. Plasma ANP then decreased so that by the end of the study the level was the same as before the saline infusion. However, at this time, 195 min after the saline infusion was stopped, there was still a net positive sodium balance of 220 mmol and urinary sodium excretion remained significantly elevated. 5. Our results are compatible with the concept that increased ANP secretion may play a role in the immediate increase in sodium excretion after a saline load. However, they also suggest that other mechanisms may be more important for the longer term increase in sodium excretion.

Impaired Natriuretic Response to Atrial Natriuretic Peptide in the Isolated Kidney of Rats with Experimental Cirrhosis

1990 ◽  
Vol 79 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Marios Z. Panos ◽  
Christopher Gove ◽  
John D. Firth ◽  
Anthony E. G. Raine ◽  
John G. G. Ledingham ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Plasma Concentrations ◽  
Urinary Sodium Excretion ◽  
Sodium Retention ◽  
Kidney Weight ◽  
Experimental Cirrhosis ◽  
Atrial Natriuretic

1. Sodium retention in cirrhosis may be partly attributable to resistance to a putative circulating natriuretic factor. In cirrhosis, plasma concentrations of atrial natriuretic peptide are often increased in the presence of sodium retention. 2. In order to determine whether the kidney of cirrhotic animals may be insensitive to atrial natriuretic peptide, isolated perfused kidneys from six cirrhotic and five control rats were exposed to increasing concentrations of atrial natriuretic peptide. Cirrhosis had been induced by carbon tetrachloride administration. 3. Excretion in vivo of a 2 mmol sodium load, administered by gavage, was impaired in cirrhotic animals for up to 4 h as compared with control animals (4.2 ± 1.9 vs34.9± 13.4% P < 0.05). 4. During perfusion at 110 mmHg in the absence of atrial natriuretic peptide, sodium excretion by isolated kidneys of cirrhotic animals tended to be lower than in control animals, but the difference was not significant (4.93 ± 1.01 vs 8.41 ± 1.48 μmol min−1 g−1 kidney weight, P = 0.09). There was a smaller increase in urinary sodium excretion by the kidneys of cirrhotic rats compared with control rats in the presence of atrial natriuretic peptide at 10, 50 and 200 pmol/l (respectively: 0.06 ± 0.08 vs 1.29 ± 0.35 μmol min−1 g−1 kidney weight, P < 0.02; 0.49 ± 0.08 vs 1.82 ± 0.42 μmol min−1 g−1 kidney weight, P < 0.03; 1.42 ± 0.16 vs 3.23 ± 0.73 μmol min−1 g−1 kidney weight, P < 0.05), but not at 1000 pmol/l. 5. In this animal model of cirrhosis, renal resistance to the natriuretic action of atrial natriuretic peptide at physiological and pathophysiological concentrations may contribute to sodium retention.

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