Bradykinin antagonism inhibits the antigrowth effect of converting enzyme inhibition in the dog myocardium after discrete transmural myocardial necrosis

Kenneth M. McDonald, James Mock, Antonio D'Aloia, Todd Parrish, Kate Hauer, Gary Francis, Arthur Stillman, Jay N. Cohn

Research output: Contribution to journalArticle

146 Citations (Scopus)

Abstract

Background: Converting enzyme inhibitor (CEI) therapy, but not angiotensin II subtype I receptor blockade, has been shown to attenuate left ventricular remodeling in the dog after transmyocardial direct current (DC) shock. The purpose of this study was to address the importance of preservation of bradykinin to the antiremodeling effect of CEI treatment in this model. Methods and Results: Twenty-four hours after DC shock, adult mongrel dogs were assigned to one of three groups: a control group; a group treated with ramipril 10 mg BID; and a group treated with ramipril 10 mg BID along with a continuous subcutaneous infusion of HOE 140, a bradykinin antagonist. To assess change in left and right ventricular structure, a magnetic resonance imaging (MRI) study was performed 4 weeks after DC shock and compared with a baseline MRI study performed before DC shock. The increase in left ventricular mass (mean±SEM) in the control group was similar to that observed in the CEI-HOE 140 group (+0.73±0.19 versus +0.75±0.18 g/kg, P=NS), but both were greater than the change in mass in the ramipril group (- 0.48±0.13 g/kg, P=.004 and P=.0005, respectively). No significant change occurred in left ventricular volume or right ventricular structure in any group. Mean arterial pressure was reduced by ramipril compared with the control group (-8±2 versus +7±2 mm Hg, P=.03), and this effect was not blunted by the addition of HOE 140 (-7±3 mm Hg). Conclusions: Prevention by ramipril of the early increase in left ventricular mass in the DC shock model appears to be related to the preservation of bradykinin.

Original languageEnglish (US)
Pages (from-to)2043-2048
Number of pages6
JournalCirculation
Volume91
Issue number7
DOIs
StatePublished - Apr 1 1995

Fingerprint

Ramipril
Bradykinin
Shock
Myocardium
Necrosis
Dogs
Enzyme Inhibitors
Enzymes
Control Groups
Magnetic Resonance Imaging
Enzyme Therapy
Subcutaneous Infusions
Ventricular Remodeling
Angiotensin II
Arterial Pressure
icatibant

Keywords

  • angiotensin
  • bradykinin
  • enzymes
  • myocardium
  • ventricles

Cite this

Bradykinin antagonism inhibits the antigrowth effect of converting enzyme inhibition in the dog myocardium after discrete transmural myocardial necrosis. / McDonald, Kenneth M.; Mock, James; D'Aloia, Antonio; Parrish, Todd; Hauer, Kate; Francis, Gary; Stillman, Arthur; Cohn, Jay N.

In: Circulation, Vol. 91, No. 7, 01.04.1995, p. 2043-2048.

Research output: Contribution to journalArticle

McDonald, Kenneth M. ; Mock, James ; D'Aloia, Antonio ; Parrish, Todd ; Hauer, Kate ; Francis, Gary ; Stillman, Arthur ; Cohn, Jay N. / Bradykinin antagonism inhibits the antigrowth effect of converting enzyme inhibition in the dog myocardium after discrete transmural myocardial necrosis. In: Circulation. 1995 ; Vol. 91, No. 7. pp. 2043-2048.
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abstract = "Background: Converting enzyme inhibitor (CEI) therapy, but not angiotensin II subtype I receptor blockade, has been shown to attenuate left ventricular remodeling in the dog after transmyocardial direct current (DC) shock. The purpose of this study was to address the importance of preservation of bradykinin to the antiremodeling effect of CEI treatment in this model. Methods and Results: Twenty-four hours after DC shock, adult mongrel dogs were assigned to one of three groups: a control group; a group treated with ramipril 10 mg BID; and a group treated with ramipril 10 mg BID along with a continuous subcutaneous infusion of HOE 140, a bradykinin antagonist. To assess change in left and right ventricular structure, a magnetic resonance imaging (MRI) study was performed 4 weeks after DC shock and compared with a baseline MRI study performed before DC shock. The increase in left ventricular mass (mean±SEM) in the control group was similar to that observed in the CEI-HOE 140 group (+0.73±0.19 versus +0.75±0.18 g/kg, P=NS), but both were greater than the change in mass in the ramipril group (- 0.48±0.13 g/kg, P=.004 and P=.0005, respectively). No significant change occurred in left ventricular volume or right ventricular structure in any group. Mean arterial pressure was reduced by ramipril compared with the control group (-8±2 versus +7±2 mm Hg, P=.03), and this effect was not blunted by the addition of HOE 140 (-7±3 mm Hg). Conclusions: Prevention by ramipril of the early increase in left ventricular mass in the DC shock model appears to be related to the preservation of bradykinin.",
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T1 - Bradykinin antagonism inhibits the antigrowth effect of converting enzyme inhibition in the dog myocardium after discrete transmural myocardial necrosis

AU - McDonald, Kenneth M.

AU - Mock, James

AU - D'Aloia, Antonio

AU - Parrish, Todd

AU - Hauer, Kate

AU - Francis, Gary

AU - Stillman, Arthur

AU - Cohn, Jay N.

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N2 - Background: Converting enzyme inhibitor (CEI) therapy, but not angiotensin II subtype I receptor blockade, has been shown to attenuate left ventricular remodeling in the dog after transmyocardial direct current (DC) shock. The purpose of this study was to address the importance of preservation of bradykinin to the antiremodeling effect of CEI treatment in this model. Methods and Results: Twenty-four hours after DC shock, adult mongrel dogs were assigned to one of three groups: a control group; a group treated with ramipril 10 mg BID; and a group treated with ramipril 10 mg BID along with a continuous subcutaneous infusion of HOE 140, a bradykinin antagonist. To assess change in left and right ventricular structure, a magnetic resonance imaging (MRI) study was performed 4 weeks after DC shock and compared with a baseline MRI study performed before DC shock. The increase in left ventricular mass (mean±SEM) in the control group was similar to that observed in the CEI-HOE 140 group (+0.73±0.19 versus +0.75±0.18 g/kg, P=NS), but both were greater than the change in mass in the ramipril group (- 0.48±0.13 g/kg, P=.004 and P=.0005, respectively). No significant change occurred in left ventricular volume or right ventricular structure in any group. Mean arterial pressure was reduced by ramipril compared with the control group (-8±2 versus +7±2 mm Hg, P=.03), and this effect was not blunted by the addition of HOE 140 (-7±3 mm Hg). Conclusions: Prevention by ramipril of the early increase in left ventricular mass in the DC shock model appears to be related to the preservation of bradykinin.

AB - Background: Converting enzyme inhibitor (CEI) therapy, but not angiotensin II subtype I receptor blockade, has been shown to attenuate left ventricular remodeling in the dog after transmyocardial direct current (DC) shock. The purpose of this study was to address the importance of preservation of bradykinin to the antiremodeling effect of CEI treatment in this model. Methods and Results: Twenty-four hours after DC shock, adult mongrel dogs were assigned to one of three groups: a control group; a group treated with ramipril 10 mg BID; and a group treated with ramipril 10 mg BID along with a continuous subcutaneous infusion of HOE 140, a bradykinin antagonist. To assess change in left and right ventricular structure, a magnetic resonance imaging (MRI) study was performed 4 weeks after DC shock and compared with a baseline MRI study performed before DC shock. The increase in left ventricular mass (mean±SEM) in the control group was similar to that observed in the CEI-HOE 140 group (+0.73±0.19 versus +0.75±0.18 g/kg, P=NS), but both were greater than the change in mass in the ramipril group (- 0.48±0.13 g/kg, P=.004 and P=.0005, respectively). No significant change occurred in left ventricular volume or right ventricular structure in any group. Mean arterial pressure was reduced by ramipril compared with the control group (-8±2 versus +7±2 mm Hg, P=.03), and this effect was not blunted by the addition of HOE 140 (-7±3 mm Hg). Conclusions: Prevention by ramipril of the early increase in left ventricular mass in the DC shock model appears to be related to the preservation of bradykinin.

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