Skip Navigation

Cardiovascular Research 1995 30(3):386-393; doi:10.1016/S0008-6363(95)00058-5
© 1995 by European Society of Cardiology
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by van Veldhuisen, D. J.
Right arrow Articles by Lie, K.I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Veldhuisen, D. J.
Right arrow Articles by Lie, K.I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1995, European Society of Cardiology

Relation between myocardial β-adrenoceptor density and hemodynamic and neurohumoral changes in a rat model of chronic myocardial infarction: effects of ibopamine and captopril

Dirk J. van Veldhuisen*,a, Otto-Erich Broddeb, c, Wiek H. van Gilsta, d, Cerstin Schulzec, Han Hegemand, Rutger L. Anthonioa, Egbert Scholtensd, Pieter A. de Graeffd, Harry Wesselingd and K.I. Liea

aDepartment of Cardiology/Thorax Center, University Hospital Groningen, Oostersingel 59, 9713 EZ Groningen, Netherlands
bBiochemical Research Laboratory, Medical Clinic and Outpatient Clinic, Division of Renal and Hypertensive Diseases, University of Essen, Essen, Germany
cInstitute of Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany
dDepartment of Pharmacology/Clinical Pharmacology, University Hospital Groningen, Groningen, Netherlands

* Corresponding author. Tel. (+31-50)612355; Fax (+31-50)614391.

Objectives: The purpose of this study was to investigate the changes in β-adrenoceptor density (Bmax) and distribution in a model of chronic myocardial infarction in rats, and to relate possible changes to hemodynamic and neurohumoral abnormalities. In addition, we examined the effects of 8 weeks treatment with ibopamine and captopril. Methods: There were 3 experiments: (1) Bmax and plasma catecholamines were examined (n = 46), (2) Bmax was compared in infarcted and non-infarcted tissue (n = 13), and (3) contractile function was evaluated by isolated heart perfusion (n = 40). Of rats in Expts. (1) and (3), 50% had myocardial infarction induced by coronary ligation and 50% were controls. Each group was divided between ibopamine, ibopamine and captopril, or standard (no drug) treatment. Results:Bmax was not decreased in rats with myocardial infarction (10.8 ± 0.8 fmol/mg protein), compared to normal rats (11.4 ± 0.6 fmol/mg protein), and the ratio β1/β2 was also unaffected. In infarcted tissue, Bmax was significantly (P = 0.03) lower than in non-infarcted tissue. Baseline left ventricular pressure, systolic and diastolic dP/dT were all impaired (P < 0.001), and plasma norepinephrine levels were elevated in rats with myocardial infarction (16.03 ± 230 vs. 1287 ± 83 pg/ml; P < 0.05), compared to normals. Both ibopamine alone and in combination with captopril reduced the elevated plasma norepinephrine levels in infarcted rats (P < 0.001), but only the combination of the 2 drugs significantly increased Bmax in infarcted rats (14.7 ± 0.8 fmol/mg protein; P = 0.03 vs. untreated myocardial infarction), while ibopamine alone had no significant effect (13.1 ±1.1 fmol/mg protein; p = ns). Also, active drug treatment had no significant effect on the hemodynamic changes. Conclusions: In this coronary artery ligation model of myocardial infarction in rats, no β-adrenoceptor down-regulation is observed, despite marked abnormalities in baseline left ventricular function and plasma norepinephrine levels. The combination of ibopamine and captopril significantly increases Bmax in infarcted rats, which is accompanied by a reduction in plasma norepinephrine levels, but not by an improvement in hemodynamic parameters.

KEYWORDS Adrenergic receptors; Heart failure; Systemic hemodynamics; RAAS; ACE inhibitors; Ibopamine; Catecholamines; Rat heart

{star} This work was presented in part at the XVth Congress of the European Society of Cardiology, August 1993, Nice, France.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.