scholarly journals Clinical importance of urinary sodium excretion in acute heart failure

2020 ◽  
Vol 22 (8) ◽  
pp. 1438-1447 ◽  
Author(s):  
Kevin Damman ◽  
Jozine M. Ter Maaten ◽  
Jenifer E. Coster ◽  
Jan A. Krikken ◽  
Vincent M. Deursen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Sodium Excretion ◽  
Clinical Importance ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium

Neurohumoral modulators and sodium balance in experimental heart failure

1993 ◽  
Vol 264 (4) ◽  
pp. H1187-H1193 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Av Fistula ◽  
Before And After ◽  
High Output Heart Failure

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.

Distinct roles for renal particulate and soluble guanylyl cyclases in preserving renal function in experimental acute heart failure

2007 ◽  
Vol 293 (4) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Fernando L. Martin ◽  
Thanom Supaporn ◽  
Horng H. Chen ◽  
Sharon M. Sandberg ◽  
Yuzuru Matsuda ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Acute Heart Failure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Therapeutic Implications ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Poor Outcomes

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.

scholarly journals Urinary sodium excretion and risk of heart failure in men and women in the EPIC-Norfolk study

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P2478-P2478
Author(s):  
R. Pfister ◽  
G. Michels ◽  
S. Sharp ◽  
R. Luben ◽  
N. Wareham ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Men And Women

Estimated urinary sodium excretion and risk of heart failure in men and women in the EPIC-Norfolk study

2014 ◽  
Vol 16 (4) ◽  
pp. 394-402 ◽  
Author(s):  
Roman Pfister ◽  
Guido Michels ◽  
Stephen J. Sharp ◽  
Robert Luben ◽  
Nick J. Wareham ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Men And Women

TIMED RECUMBENCY AND LOOP DIURETIC DOSING ON URINARY SODIUM EXCRETION IN HEART FAILURE.

2004 ◽  
Vol 52 ◽  
pp. S289
Author(s):  
J E Klemis ◽  
R N Khouzam ◽  
B M Wall ◽  
T A Mangold ◽  
K T Weber
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Loop Diuretic ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium

Effect of Timed Semirecumbency and Furosemide Dosing on Urinary Sodium Excretion in Patients with Compensated Heart Failure

2006 ◽  
Vol 332 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Rami N. Khouzam ◽  
Maeda D. Nelson ◽  
Jimmy E. Klemis ◽  
Karl T. Weber ◽  
Barry M. Wall ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium

Cardiovascular and renal effects of adrenomedullin in rats with heart failure

1999 ◽  
Vol 276 (1) ◽  
pp. R213-R218 ◽  
Author(s):  
Noritoshi Nagaya ◽  
Toshio Nishikimi ◽  
Takeshi Horio ◽  
Fumiki Yoshihara ◽  
Akio Kanazawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Systolic Pressure ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
High Dose ◽  
Renal Effects

Plasma adrenomedullin (AM), a novel hypotensive peptide, has been shown to increase in heart failure (HF). This study sought to examine the cardiovascular and renal effects of intravenous infusion of AM in HF rats and sham-operated rats (control) using two doses of AM that would not induce hypotension. Rat AM-(1—50) was intravenously administered at rates of 0.01 (low) and 0.05 (high) μg ⋅ kg body wt−1 ⋅ min−1. Low-dose AM increased urine flow (+21% in HF, +29% in control) and urinary sodium excretion (+109% in HF, +123% in control) without changes in any hemodynamic variables. In contrast, high-dose AM slightly decreased mean arterial pressure (−3% in HF, −5% in control) and significantly increased cardiac output (+20% in HF, +12% in control). Infusion of high-dose AM resulted in significant decreases in right ventricular systolic pressure (−11%) and right atrial pressure (−28%) only in HF rats. High-dose AM significantly increased glomerular filtration rate (+10% in HF, +16% in control) and effective renal plasma flow (+25% in HF, +46% in control) as well as urine flow and urinary sodium excretion. In summary, intravenous infusion of AM exerted diuresis and natriuresis without inducing hypotension and, in the higher dose, produced beneficial hemodynamic and renal vasodilator effects in rats with compensated HF.

Urinary Sodium Excretion and Proximal Tubule Reabsorption in Rats with High-Output Heart Failure

Nephron ◽  
1974 ◽  
Vol 12 (4) ◽  
pp. 261-274 ◽  
Author(s):  
Klaus O. Stumpe ◽  
B. Reinelt ◽  
C. Ressel ◽  
H. Klein ◽  
F. Krück
Keyword(s):  
Heart Failure ◽  
Proximal Tubule ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Output Heart Failure ◽  
High Output
Sign in / Sign up

Export Citation Format

Share Document