The modulating actions of sulfonylurea on atrial natriuretic peptide release in experimental acute heart failure

Horng H. Chen, Karen Oh, Andre Terzic, John C. Burnett

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Objectives: This study defined the modulating actions of sulfonylurea on acute release of atrial natriuretic peptide (ANP) in experimental acute heart failure. Background: Sulfonylurea drugs, blockers of cardioprotective ATP- sensitive K+ (K(ATP)) channels, may increase the risk of early cardiovascular mortality. In cardiovascular diseases such as acute heart failure, early release of ANP is essential for cardiorenal homeostasis. Although K(ATP) channels regulate secretion of hormones, such as insulin, it is unknown whether sulfonylureas interfere with ANP release in acute heart failure. Methods: The effects of acute administration of glyburide (0.3 mg/kg), a prototype sulfonylurea, on ANP release and sodium excretion were measured in vivo in a canine model of pacing-induced acute heart failure characterized by acute atrial stretch. Immunoreactivity, in atrial tissue, for ANP and the K(ATP) channel subunit, Kir6.2, was determined using specific antibodies. Results: With increased left atrial pressure in heart failure, plasma levels of ANP increased rapidly and peaked within 25 ± 3 min. Glyburide delayed the time required for peak plasma ANP secretion to 48 ± 5 min. This resulted in reduced natriuresis from 84 ± 17 μEq/min in the absence of glyburide, to 34 ± 9 μEq/min in the presence of glyburide. However, glyburide did not alter the renal natriuretic responsiveness to exogenously administered ANP in normal dogs. In atrial tissue, both ANP and the K(ATP) channel subunit, Kir6.2, displayed strong immunoreactivity and co- localization. Conclusions: Glyburide delays release of ANP in acute heart failure resulting in impaired natriuresis. This cannot be ascribed to an antinatriuretic effect on the kidney, but rather may be due to interference with K(ATP) channel-dependent ANP secretion from the atrium. Such adverse outcome of sulfonylurea drug use could reduce the compensatory capacity to preserve cardiorenal homeostasis in acute heart failure. (C) 2000 European Society of Cardiology.

Original languageEnglish (US)
Pages (from-to)33-40
Number of pages8
JournalEuropean Journal of Heart Failure
Volume2
Issue number1
DOIs
StatePublished - Mar 1 2000
Externally publishedYes

Fingerprint

Atrial Natriuretic Factor
Heart Failure
Glyburide
Adenosine Triphosphate
Natriuresis
Homeostasis
Kidney
Atrial Pressure
Pharmaceutical Preparations
Canidae
Cardiovascular Diseases
Sodium
Hormones
Dogs
Insulin

Keywords

  • ATP-sensitive K channel
  • Cardioprotection
  • Kidney
  • Kir6.2
  • Natriuresis
  • Sulfonylurea

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

The modulating actions of sulfonylurea on atrial natriuretic peptide release in experimental acute heart failure. / Chen, Horng H.; Oh, Karen; Terzic, Andre; Burnett, John C.

In: European Journal of Heart Failure, Vol. 2, No. 1, 01.03.2000, p. 33-40.

Research output: Contribution to journalArticle

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N2 - Objectives: This study defined the modulating actions of sulfonylurea on acute release of atrial natriuretic peptide (ANP) in experimental acute heart failure. Background: Sulfonylurea drugs, blockers of cardioprotective ATP- sensitive K+ (K(ATP)) channels, may increase the risk of early cardiovascular mortality. In cardiovascular diseases such as acute heart failure, early release of ANP is essential for cardiorenal homeostasis. Although K(ATP) channels regulate secretion of hormones, such as insulin, it is unknown whether sulfonylureas interfere with ANP release in acute heart failure. Methods: The effects of acute administration of glyburide (0.3 mg/kg), a prototype sulfonylurea, on ANP release and sodium excretion were measured in vivo in a canine model of pacing-induced acute heart failure characterized by acute atrial stretch. Immunoreactivity, in atrial tissue, for ANP and the K(ATP) channel subunit, Kir6.2, was determined using specific antibodies. Results: With increased left atrial pressure in heart failure, plasma levels of ANP increased rapidly and peaked within 25 ± 3 min. Glyburide delayed the time required for peak plasma ANP secretion to 48 ± 5 min. This resulted in reduced natriuresis from 84 ± 17 μEq/min in the absence of glyburide, to 34 ± 9 μEq/min in the presence of glyburide. However, glyburide did not alter the renal natriuretic responsiveness to exogenously administered ANP in normal dogs. In atrial tissue, both ANP and the K(ATP) channel subunit, Kir6.2, displayed strong immunoreactivity and co- localization. Conclusions: Glyburide delays release of ANP in acute heart failure resulting in impaired natriuresis. This cannot be ascribed to an antinatriuretic effect on the kidney, but rather may be due to interference with K(ATP) channel-dependent ANP secretion from the atrium. Such adverse outcome of sulfonylurea drug use could reduce the compensatory capacity to preserve cardiorenal homeostasis in acute heart failure. (C) 2000 European Society of Cardiology.

AB - Objectives: This study defined the modulating actions of sulfonylurea on acute release of atrial natriuretic peptide (ANP) in experimental acute heart failure. Background: Sulfonylurea drugs, blockers of cardioprotective ATP- sensitive K+ (K(ATP)) channels, may increase the risk of early cardiovascular mortality. In cardiovascular diseases such as acute heart failure, early release of ANP is essential for cardiorenal homeostasis. Although K(ATP) channels regulate secretion of hormones, such as insulin, it is unknown whether sulfonylureas interfere with ANP release in acute heart failure. Methods: The effects of acute administration of glyburide (0.3 mg/kg), a prototype sulfonylurea, on ANP release and sodium excretion were measured in vivo in a canine model of pacing-induced acute heart failure characterized by acute atrial stretch. Immunoreactivity, in atrial tissue, for ANP and the K(ATP) channel subunit, Kir6.2, was determined using specific antibodies. Results: With increased left atrial pressure in heart failure, plasma levels of ANP increased rapidly and peaked within 25 ± 3 min. Glyburide delayed the time required for peak plasma ANP secretion to 48 ± 5 min. This resulted in reduced natriuresis from 84 ± 17 μEq/min in the absence of glyburide, to 34 ± 9 μEq/min in the presence of glyburide. However, glyburide did not alter the renal natriuretic responsiveness to exogenously administered ANP in normal dogs. In atrial tissue, both ANP and the K(ATP) channel subunit, Kir6.2, displayed strong immunoreactivity and co- localization. Conclusions: Glyburide delays release of ANP in acute heart failure resulting in impaired natriuresis. This cannot be ascribed to an antinatriuretic effect on the kidney, but rather may be due to interference with K(ATP) channel-dependent ANP secretion from the atrium. Such adverse outcome of sulfonylurea drug use could reduce the compensatory capacity to preserve cardiorenal homeostasis in acute heart failure. (C) 2000 European Society of Cardiology.

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