Brain Natriuretic Peptide Enhances Renal Actions of Furosemide and Suppresses Furosemide-Induced Aldosterone Activation in Experimental Heart Failure

Alessandro Cataliotti, Guido Boerrigter, Lisa C. Costello-Boerrigter, John A. Schirger, Toshihiro Tsuruda, Denise M. Heublein, Horng Haur Chen, Lorenzo S. Malatino, John C Jr. Burnett

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Abstract

Background - The renal actions of brain natriuretic peptide (BNP) in congestive heart failure (CHF) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR), and lack of activation of the renin-angiotensin-aldosterone system (RAAS). In contrast, diuretic- induced natriuresis may be associated with reduced GFR and RAAS activation. The objective of this study was to test the hypothesis that exogenous BNP enhances the renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosterone in a model of CHF. Methods and Results - CHF was produced in 2 groups of dogs by ventricular pacing. One group received continuous (90-minute) intravenous Fs (1 mg · kg-1 · h-1). A second group (Fs+BNP) received 45-minute intravenous coinfusion of Fs (1 mg · kg-1 · h-1) and low-dose (2 pmol · kg-1 · min-1) BNP followed by 45-minute coinfusion of Fs (1 mg · kg-1 · h-1) and high-dose (10 pmol · kg-1 · min-1) BNP. Fs increased urinary flow, but the effect of Fs+BNP was greater. Similarly, urinary sodium excretion was higher in the Fs+BNP group. Although GFR tended to decrease in the Fs group, it increased in the Fs+BNP group (35±3 to 56±4*) (* indicates P<0.05 versus baseline) (P<0.0001 between groups). Plasma aldosterone increased with Fs (41±10 to 100±11* ng/dL) but was attenuated in the Fs+BNP group (44±11 to 54±9 ng/dL low-dose and to 47±7 ng/dL high-dose) (P=0.0007 between groups). Conclusions - Fs+BNP has more profound diuretic and natriuretic responses than Fs alone and also increases GFR without activation of aldosterone. Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function and inhibiting activation of aldosterone.

Original languageEnglish (US)
Pages (from-to)1680-1685
Number of pages6
JournalCirculation
Volume109
Issue number13
DOIs
StatePublished - Apr 6 2004

Fingerprint

Brain Natriuretic Peptide
Furosemide
Aldosterone
Heart Failure
Kidney
Glomerular Filtration Rate
Natriuresis
Diuretics
Diuresis
Renin-Angiotensin System
Sodium Potassium Chloride Symporter Inhibitors

Keywords

  • Diuretics
  • Glomerular filtration rate
  • Natriuretic peptide, brain
  • Renin-angiotensin system

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Brain Natriuretic Peptide Enhances Renal Actions of Furosemide and Suppresses Furosemide-Induced Aldosterone Activation in Experimental Heart Failure. / Cataliotti, Alessandro; Boerrigter, Guido; Costello-Boerrigter, Lisa C.; Schirger, John A.; Tsuruda, Toshihiro; Heublein, Denise M.; Chen, Horng Haur; Malatino, Lorenzo S.; Burnett, John C Jr.

In: Circulation, Vol. 109, No. 13, 06.04.2004, p. 1680-1685.

Research output: Contribution to journalArticle

Cataliotti, Alessandro ; Boerrigter, Guido ; Costello-Boerrigter, Lisa C. ; Schirger, John A. ; Tsuruda, Toshihiro ; Heublein, Denise M. ; Chen, Horng Haur ; Malatino, Lorenzo S. ; Burnett, John C Jr. / Brain Natriuretic Peptide Enhances Renal Actions of Furosemide and Suppresses Furosemide-Induced Aldosterone Activation in Experimental Heart Failure. In: Circulation. 2004 ; Vol. 109, No. 13. pp. 1680-1685.
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abstract = "Background - The renal actions of brain natriuretic peptide (BNP) in congestive heart failure (CHF) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR), and lack of activation of the renin-angiotensin-aldosterone system (RAAS). In contrast, diuretic- induced natriuresis may be associated with reduced GFR and RAAS activation. The objective of this study was to test the hypothesis that exogenous BNP enhances the renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosterone in a model of CHF. Methods and Results - CHF was produced in 2 groups of dogs by ventricular pacing. One group received continuous (90-minute) intravenous Fs (1 mg · kg-1 · h-1). A second group (Fs+BNP) received 45-minute intravenous coinfusion of Fs (1 mg · kg-1 · h-1) and low-dose (2 pmol · kg-1 · min-1) BNP followed by 45-minute coinfusion of Fs (1 mg · kg-1 · h-1) and high-dose (10 pmol · kg-1 · min-1) BNP. Fs increased urinary flow, but the effect of Fs+BNP was greater. Similarly, urinary sodium excretion was higher in the Fs+BNP group. Although GFR tended to decrease in the Fs group, it increased in the Fs+BNP group (35±3 to 56±4*) (* indicates P<0.05 versus baseline) (P<0.0001 between groups). Plasma aldosterone increased with Fs (41±10 to 100±11* ng/dL) but was attenuated in the Fs+BNP group (44±11 to 54±9 ng/dL low-dose and to 47±7 ng/dL high-dose) (P=0.0007 between groups). Conclusions - Fs+BNP has more profound diuretic and natriuretic responses than Fs alone and also increases GFR without activation of aldosterone. Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function and inhibiting activation of aldosterone.",
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T1 - Brain Natriuretic Peptide Enhances Renal Actions of Furosemide and Suppresses Furosemide-Induced Aldosterone Activation in Experimental Heart Failure

AU - Cataliotti, Alessandro

AU - Boerrigter, Guido

AU - Costello-Boerrigter, Lisa C.

AU - Schirger, John A.

AU - Tsuruda, Toshihiro

AU - Heublein, Denise M.

AU - Chen, Horng Haur

AU - Malatino, Lorenzo S.

AU - Burnett, John C Jr.

PY - 2004/4/6

Y1 - 2004/4/6

N2 - Background - The renal actions of brain natriuretic peptide (BNP) in congestive heart failure (CHF) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR), and lack of activation of the renin-angiotensin-aldosterone system (RAAS). In contrast, diuretic- induced natriuresis may be associated with reduced GFR and RAAS activation. The objective of this study was to test the hypothesis that exogenous BNP enhances the renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosterone in a model of CHF. Methods and Results - CHF was produced in 2 groups of dogs by ventricular pacing. One group received continuous (90-minute) intravenous Fs (1 mg · kg-1 · h-1). A second group (Fs+BNP) received 45-minute intravenous coinfusion of Fs (1 mg · kg-1 · h-1) and low-dose (2 pmol · kg-1 · min-1) BNP followed by 45-minute coinfusion of Fs (1 mg · kg-1 · h-1) and high-dose (10 pmol · kg-1 · min-1) BNP. Fs increased urinary flow, but the effect of Fs+BNP was greater. Similarly, urinary sodium excretion was higher in the Fs+BNP group. Although GFR tended to decrease in the Fs group, it increased in the Fs+BNP group (35±3 to 56±4*) (* indicates P<0.05 versus baseline) (P<0.0001 between groups). Plasma aldosterone increased with Fs (41±10 to 100±11* ng/dL) but was attenuated in the Fs+BNP group (44±11 to 54±9 ng/dL low-dose and to 47±7 ng/dL high-dose) (P=0.0007 between groups). Conclusions - Fs+BNP has more profound diuretic and natriuretic responses than Fs alone and also increases GFR without activation of aldosterone. Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function and inhibiting activation of aldosterone.

AB - Background - The renal actions of brain natriuretic peptide (BNP) in congestive heart failure (CHF) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR), and lack of activation of the renin-angiotensin-aldosterone system (RAAS). In contrast, diuretic- induced natriuresis may be associated with reduced GFR and RAAS activation. The objective of this study was to test the hypothesis that exogenous BNP enhances the renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosterone in a model of CHF. Methods and Results - CHF was produced in 2 groups of dogs by ventricular pacing. One group received continuous (90-minute) intravenous Fs (1 mg · kg-1 · h-1). A second group (Fs+BNP) received 45-minute intravenous coinfusion of Fs (1 mg · kg-1 · h-1) and low-dose (2 pmol · kg-1 · min-1) BNP followed by 45-minute coinfusion of Fs (1 mg · kg-1 · h-1) and high-dose (10 pmol · kg-1 · min-1) BNP. Fs increased urinary flow, but the effect of Fs+BNP was greater. Similarly, urinary sodium excretion was higher in the Fs+BNP group. Although GFR tended to decrease in the Fs group, it increased in the Fs+BNP group (35±3 to 56±4*) (* indicates P<0.05 versus baseline) (P<0.0001 between groups). Plasma aldosterone increased with Fs (41±10 to 100±11* ng/dL) but was attenuated in the Fs+BNP group (44±11 to 54±9 ng/dL low-dose and to 47±7 ng/dL high-dose) (P=0.0007 between groups). Conclusions - Fs+BNP has more profound diuretic and natriuretic responses than Fs alone and also increases GFR without activation of aldosterone. Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function and inhibiting activation of aldosterone.

KW - Diuretics

KW - Glomerular filtration rate

KW - Natriuretic peptide, brain

KW - Renin-angiotensin system

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