Activation of myocardial and renal natriuretic peptides during acute intravascular volume overload in dogs

Functional cardiorenal responses to receptor antagonism

Daniel Dean Borgeson, Tracy L. Stevens, Denise M. Heublein, Yuzuru Matsuda, John C Jr. Burnett

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

1. A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2. Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right: atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0 ± 4.2 versus 62 ± 8.0 pg/min, P < 0.05). 3. In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6 ± 1.1 to 5.0 ± 1.2 pmol/ml, P < 0.05). A significant attenuation of natriuresis (566 ± 91 versus 124 ± 198 μEq/min, P < 0.05) and diuresis (4.8 ± 0.7 versus 10.1 ± 2.0 ml/min, P < 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4. These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.

Original languageEnglish (US)
Pages (from-to)195-202
Number of pages8
JournalClinical Science
Volume95
Issue number2
StatePublished - 1998

Fingerprint

C-Type Natriuretic Peptide
Natriuretic Peptides
Atrial Natriuretic Factor
Brain Natriuretic Peptide
Dogs
Kidney
Pulmonary Wedge Pressure
Atrial Pressure
Peptide Receptors
Natriuresis
Diuresis
Diuretics
Cardiac Output
Pulmonary Artery
Epithelial Cells
Body Weight
Pressure
Control Groups
polypeptide C
HS 142-1

Keywords

  • Natriuresis
  • Natriuretic peptides
  • Volume expansion

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Activation of myocardial and renal natriuretic peptides during acute intravascular volume overload in dogs : Functional cardiorenal responses to receptor antagonism. / Borgeson, Daniel Dean; Stevens, Tracy L.; Heublein, Denise M.; Matsuda, Yuzuru; Burnett, John C Jr.

In: Clinical Science, Vol. 95, No. 2, 1998, p. 195-202.

Research output: Contribution to journalArticle

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abstract = "1. A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2. Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10{\%} of body weight over 1 h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right: atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0 ± 4.2 versus 62 ± 8.0 pg/min, P < 0.05). 3. In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6 ± 1.1 to 5.0 ± 1.2 pmol/ml, P < 0.05). A significant attenuation of natriuresis (566 ± 91 versus 124 ± 198 μEq/min, P < 0.05) and diuresis (4.8 ± 0.7 versus 10.1 ± 2.0 ml/min, P < 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4. These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.",
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AU - Stevens, Tracy L.

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AU - Matsuda, Yuzuru

AU - Burnett, John C Jr.

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AB - 1. A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2. Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right: atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0 ± 4.2 versus 62 ± 8.0 pg/min, P < 0.05). 3. In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6 ± 1.1 to 5.0 ± 1.2 pmol/ml, P < 0.05). A significant attenuation of natriuresis (566 ± 91 versus 124 ± 198 μEq/min, P < 0.05) and diuresis (4.8 ± 0.7 versus 10.1 ± 2.0 ml/min, P < 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4. These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.

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