Urinary sodium evaluation: the missing target for diuretic treatment optimization in acute heart failure patients? Letter regarding the article ‘Clinical importance of urinary sodium excretion in acute heart failure’

2020 ◽  
Vol 22 (10) ◽  
pp. 1933-1933
Author(s):  
Alessandro Galluzzo ◽  
Maurizio Bertaina ◽  
Simone Frea
2020 ◽  
Vol 22 (8) ◽  
pp. 1438-1447 ◽  
Author(s):  
Kevin Damman ◽  
Jozine M. Ter Maaten ◽  
Jenifer E. Coster ◽  
Jan A. Krikken ◽  
Vincent M. Deursen ◽  
...  

2016 ◽  
Vol 22 (9) ◽  
pp. S226
Author(s):  
Yuichiro Iida ◽  
Takayuki Inomata ◽  
Toyoji Kaida ◽  
Teppei Fujita ◽  
Yuki Ikeda ◽  
...  

1993 ◽  
Vol 264 (4) ◽  
pp. H1187-H1193 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson

The acute and chronic interactions of the renal nerves, atrial natriuretic factor (ANF), and mineralocorticoids for the regulation of sodium balance were examined in dogs with an arteriovenous (AV) fistula and the syndrome of high-output heart failure (HOHF) (n = 6). After the AV fistula and bilateral renal denervation, the animals avidly retained sodium for 5-7 days and then regained sodium balance for the subsequent 3 wk. This compensation was associated with the sustained elevations of plasma ANF and the normalization of plasma renin. Subsequent administration of deoxycorticosterone acetate (DOCA) for 10 days produced consistent sodium retention despite additional elevations in plasma ANF. All of these responses were similar to previous studies in AV fistula dogs with intact renal nerves. In a separate part of the study, the renal actions of acute synthetic ANF infusions were examined in these renal-denervated AV fistula dogs before and after DOCA. In the pre-DOCA experiments, ANF infusions at 15, 30, and 100 ng.kg-1.min-1 produced dose-related increases in urinary sodium excretion and significant elevations in creatinine clearance. In the presence of DOCA, urinary sodium excretion was markedly attenuated during identical ANF infusions. The composite results suggest that mineralocorticoids have an important modulatory role for the regulation of sodium balance in experimental HOHF. However, compared with earlier studies in compensated AV fistula dogs with intact renal nerves, the present studies demonstrate that blockade of efferent renal sympathetic nerve activity can restore the natriuretic expression of acute elevations in circulating ANF.


PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0141336 ◽  
Author(s):  
Matthias Hammon ◽  
Susan Grossmann ◽  
Peter Linz ◽  
Christoph Kopp ◽  
Anke Dahlmann ◽  
...  

2007 ◽  
Vol 293 (4) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Fernando L. Martin ◽  
Thanom Supaporn ◽  
Horng H. Chen ◽  
Sharon M. Sandberg ◽  
Yuzuru Matsuda ◽  
...  

Worsening renal function in the setting of human acute heart failure (AHF) predicts poor outcomes, such as rehospitalization and increased mortality. Understanding potential renoprotective mechanisms is warranted. The guanylate cyclase (GC) enzymes and their second messenger cGMP are the target of two important circulating neurohumoral systems with renoprotective properties. Specifically, natriuretic peptides (NP) released from the heart with AHF target particulate GC in the kidney, while the nitric oxide (NO) system is an activator of renal soluble GC. We hypothesized that both systems are essential to preserve renal excretory and hemodynamic function in AHF but with distinct roles. We investigated these roles in three groups of anesthetized dogs (6 each) with AHF induced by rapid ventricular pacing. After a baseline AHF clearance, each group received intrarenal vehicle (control), NG-monomethyl-l-arginine (l-NMMA), a competitive NO inhibitor (50 μg·kg−1·min−1) or a specific NP receptor antagonist, HS-142-1 (0.5 mg/kg). We observed that intrarenal l-NMMA decreased renal blood flow (RBF) without significant decreases in glomerular filtration rate (GFR), urinary sodium excretion (UNaV), or urinary cGMP. In contrast, HS-142-1 resulted in a decrease in UNaV and cGMP excretion together with a reduction in GFR and an increase in distal fractional tubular sodium reabsorption. We conclude that in AHF, the NP system plays a role in maintaining sodium excretion and GFR, while the function of NO is in the maintenance of RBF. These studies have both physiological and therapeutic implications warranting further research into cardiorenal interactions in this syndrome of AHF.


2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P2478-P2478
Author(s):  
R. Pfister ◽  
G. Michels ◽  
S. Sharp ◽  
R. Luben ◽  
N. Wareham ◽  
...  

2014 ◽  
Vol 16 (4) ◽  
pp. 394-402 ◽  
Author(s):  
Roman Pfister ◽  
Guido Michels ◽  
Stephen J. Sharp ◽  
Robert Luben ◽  
Nick J. Wareham ◽  
...  

2004 ◽  
Vol 52 ◽  
pp. S289
Author(s):  
J E Klemis ◽  
R N Khouzam ◽  
B M Wall ◽  
T A Mangold ◽  
K T Weber

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