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

vanVeldhuisen, DJ; Brodde, O.‐E.; Vangilst, Wh; Schulze, Christopher; Anthonio, RL; Degraeff, Pa; Wesseling, H; Lie, Ki

doi:10.1016/s0008-6363(95)00058-5

Cited by 8 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the rat infarct model, myocardial ␤-AR have been found to be preserved, 10,28 -31 downregulated, 7 or even upregulated. 18 Unlike Sethi et al, 7 who found that ␤-AR downregulation correlated well with the extent of hemodynamic dysfunction, we could not confirm these findings despite profound global and regional contractile dysfunction in our rats. It is unclear whether they studied only the remote noninfarcted myocardium.…”

Section: ␤-Ar Modulation In Postinfarction Remodelingcontrasting

confidence: 99%

See 1 more Smart Citation

Myocyte Response to β-Adrenergic Stimulation Is Preserved in the Noninfarcted Myocardium of Globally Dysfunctional Rat Hearts After Myocardial Infarction

2000

View full text Add to dashboard Cite

show abstract

Section: ␤-Ar Modulation In Postinfarction Remodelingcontrasting

confidence: 99%

“…6,18 Myocyte loss as a result of MI and consequent ventricular dilation and increased wall stress could explain some of the diminished contractile response in isolated heart preparations. This, however, cannot explain the attenuated contractile response to ISO reported in noninfarcted isolated papillary muscle.…”

Section: Myocyte Function In Remodeled Myocardiummentioning

confidence: 99%

Myocyte Response to β-Adrenergic Stimulation Is Preserved in the Noninfarcted Myocardium of Globally Dysfunctional Rat Hearts After Myocardial Infarction

2000

View full text Add to dashboard Cite

show abstract

“…In rats with MI, a significant reduction of β-receptor density was reported 33,34) and ACE inhibitor treatment restored the reduction. 33) However, others 35,36) have reported no significant changes in β-receptor density in heart failure after MI, as seen in the present study. These differences may not be due to the period of examination because no β-receptor downregulation was observed in 24 weeks after MI in one of our previous studies.…”

Section: Discussioncontrasting

confidence: 63%

Effects of the Angiotensin-converting Enzyme Inhibitor Enalapril on Sympathetic Neuronal Function and .BETA.-adrenergic Desensitization in Heart Failure after Myocardial Infarction in Rats.

et al. 2002

View full text Add to dashboard Cite

SUMMARYOne of the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure may derive from sympathoinhibition and the prevention of β-adrenergic desensitization. However, the roles of these properties in the overall effects of ACE inhibitor are not clear. We studied the effects of chronic enalapril treatment (20 mg/L in drinking water for 12 weeks) on left ventricular (LV) function, cardiac norepinephrine (NE), sympathetic neuronal function assessed by 131 I-metaiodobenzylguanidine (MIBG), β-receptors, and isometric contraction of papillary muscle in rats with myocardial infarction (MI) induced by coronary artery ligation. Decreased LV function in the MI rats was associated with reduced cardiac NE content and MIBG uptake, and severely blunted responses of non-infarcted papillary muscle to isoproterenol, forskolin, and calcium. Enalapril attenuated LV remodeling in association with a reduction of the ventricular loading condition and restored baseline developed tension of non-infarcted papillary muscle to the level of sham-operated rats. However, enalapril did not improve cardiac NE content, MIBG uptake, or inotropic responsiveness to β-agonists. These results suggest that the major effect of the ACE inhibitor enalapril in the treatment of heart failure is not due to sympathoinhibition or restoration of β-adrenergic pathway in this model of heart failure. (Jpn Heart J 2002; 43: 675-688)

show abstract

“…The possibility that the reduction shown in the present study could be related to decreased ß-adrenergic receptor density limited to the scar and neighboring tissue (4,24) is not likely since we removed the scars before homogenization of the left ventricles.…”

Section: Depressed ß-Adrenergic Response In Postinfarction Myocytesmentioning

confidence: 81%

“…Also, the increase in the peak amplitude of [Ca 2+ ] i transients induced by ß-adrenergic stimulation has been shown to be attenuated (5) or augmented (22) in postinfarction myocytes. Binding experiments showed even more diverse results, i.e., maintained (22)(23)(24)(25), reduced (6,8,18) or increased (26) ß-adrenergic receptor density.…”

Section: Introductionmentioning

confidence: 99%

Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure

Saraiva

Chedid

Masuda

2003

Braz J Med Biol Res

View full text Add to dashboard Cite

Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased ß-adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L) ), and the mechanisms underlying the decreased ß-adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca 2+ ] i ) transients, and the effects of ß-adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca 2+ ] i transients were investigated via fura-2 fluorescence. ß-Adrenergic receptor density was determined by [ 3 H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 ± 0.28 vs 7.6 ± 0.32 pA/pF) and a 19% reduction in mean peak [Ca 2+ ] i transients (0.13 ± 0.007 vs 0.16 ± 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (E max : 63.6 ± 4.3 vs 123.3 ± 0.9% in sham myocytes), but EC 50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca 2+ ] i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. ß-Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (B max : 93.89 ± 20.22 vs 271.5 ± 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca 2+ ] i transients. The response to ß-adrenergic stimulation was also reduced and was probably related to ß-adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.

show abstract

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

Cited by 8 publications

References 0 publications

Myocyte Response to β-Adrenergic Stimulation Is Preserved in the Noninfarcted Myocardium of Globally Dysfunctional Rat Hearts After Myocardial Infarction

Myocyte Response to β-Adrenergic Stimulation Is Preserved in the Noninfarcted Myocardium of Globally Dysfunctional Rat Hearts After Myocardial Infarction

Effects of the Angiotensin-converting Enzyme Inhibitor Enalapril on Sympathetic Neuronal Function and .BETA.-adrenergic Desensitization in Heart Failure after Myocardial Infarction in Rats.

Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure

Contact Info

Product

Resources

About