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

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Clinical importance of urinary sodium excretion in acute heart failure

European Journal of Heart Failure ◽

10.1002/ejhf.1753 ◽

2020 ◽

Vol 22 (8) ◽

pp. 1438-1447 ◽

Cited By ~ 6

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

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

European Heart Journal ◽

10.1093/eurheartj/eht308.p2478 ◽

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

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

European Journal of Heart Failure ◽

10.1002/ejhf.56 ◽

2014 ◽

Vol 16 (4) ◽

pp. 394-402 ◽

Cited By ~ 52

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

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

Journal of Investigative Medicine ◽

10.1097/00042871-200401001-00735 ◽

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

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Cardiovascular and renal effects of adrenomedullin in rats with heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.1.r213 ◽

1999 ◽

Vol 276 (1) ◽

pp. R213-R218 ◽

Cited By ~ 13

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.

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