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Enalaprilat attenuates ischemic rises in intracellular sodium in the isolated rat heart via the bradykinin receptor

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance, 2001, Vol.3(1), pp.27-34 [Peer Reviewed Journal]

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  • Title:
    Enalaprilat attenuates ischemic rises in intracellular sodium in the isolated rat heart via the bradykinin receptor
  • Author: Whang, J ; Ramasamy, R ; Dizon, J M ; Bergmann, S R
  • Found In: Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance, 2001, Vol.3(1), pp.27-34 [Peer Reviewed Journal]
  • Subjects: Magnetic Resonance Spectroscopy ; Enalaprilat -- Pharmacology ; Intracellular Fluid -- Metabolism ; Myocardial Ischemia -- Physiopathology ; Receptors, Bradykinin -- Drug Effects ; Sodium -- Metabolism
  • Language: English
  • Description: Angiotensin-converting enzyme (ACE) inhibitors have been shown to have beneficial effects on ischemic myocardium. We examined whether the ACE inhibitor, enalaprilat (EN), improves intracellular sodium homeostasis during myocardial ischemia and the relationship of this effect to bradykinin. EN (3.2 nM) was administered to isolated rat hearts that were subjected to ischemia and reperfusion. Intracellular sodium and pH were monitored using magnetic resonance spectroscopy (MRS). The specific bradykinin B2 receptor antagonist, HOE 140 (10 nM), was administered with EN in some hearts to determine the effect of bradykinin blockade on EN-mediated effects. EN blunted the rise in ischemic intracellular sodium, measured using MRS. With reperfusion, EN-treated hearts recovered 80% of their preischemic ventricular function, compared with negligible recover, in controls. These beneficial effects of EN were blocked when the bradykinin receptor antagonist, HOE 140, was coadministered with EN. HOE 140 also blocked EN-mediated attenuation of ischemic intracellular acidosis. These results suggest that EN exerts beneficial effects on ischemic intracellular sodium and pH homeostasis via the bradykinin receptor. These effects of EN may provide a mechanism for the beneficial actions of this agent during ischemia.
  • Identifier: ISSN: 1097-6647 ; PMID: 11545137 Version:1

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