2002
DOI: 10.1016/s0014-2999(02)02643-2
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Toxic cardiac effects of catecholamines: role of β-adrenoceptor downregulation

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Cited by 43 publications
(27 citation statements)
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“…It has been reported than chronic isoproterenol infusion elicits alterations in cardiac gene expression that are consistent with the development of myocyte hypertrophy and interstitial fibrosis [16], and that these deleterious effects could be mediated by b 1 -adrenoceptor stimulation [17], so b-blockade could have beneficial effects on this pathology.…”
Section: Discussionmentioning
confidence: 93%
See 1 more Smart Citation
“…It has been reported than chronic isoproterenol infusion elicits alterations in cardiac gene expression that are consistent with the development of myocyte hypertrophy and interstitial fibrosis [16], and that these deleterious effects could be mediated by b 1 -adrenoceptor stimulation [17], so b-blockade could have beneficial effects on this pathology.…”
Section: Discussionmentioning
confidence: 93%
“…Nebivolol was able to decrease ventricular collagen deposition after 6 months of treatment and this beneficial effect persisted after a long period of therapy withdrawal. Nebivolol shares vasodilating properties with other selective b 1 -blockers such as carvedilol, celiprolol or metoprolol, which are able to regress myocardial hypertrophy and fibrosis through the NO signaling pathway [17,[29][30][31], although other properties, such as the counteracting of reactive oxygen species, could not be discarded [32]. It seems that nebivolol treatment could induce persistent modifications, perhaps improving endothelium integrity of coronary vessels, that would justify a better blood flow and the decrease in collagen content observed after 3 months of drug withdrawal.…”
Section: Discussionmentioning
confidence: 99%
“…Other studies with similar dose regimens show variations in survival, cardiotoxicity, symptomatology, and strain dependence (e.g., preexisting hypertension appears to enhance the cardiotoxicity of ISO administration). Importantly, chronic and subchronic administration of very low doses of ISO may mimic natural HF pathogenesis more accurately than large acute doses because they can elicit necrosis and fibrotic cardiomyopathy through free radical-induced extracellular matrix biosynthesis [150,[155][156][157]. SD rats injected with 0.04-0.1 mg/kg/day ISO for 3-7 months had very limited sudden cardiac death and several strong similarities to a subgroup of aortic banded rats showing overt signs of HF: impaired myocardial collagen cross-linking, LV chamber dilatation, an equivalent reduction in FS, and impaired LV developed pressure-volume relations [52] as well as marked apoptosis and b 1 and b 2 AR inotropic downregulation [158].…”
Section: Pharmacological Modelsmentioning
confidence: 99%
“…These sections were stained with hematoxylin and eosin (H&E). [136] www.wjpps.com Vol 6, Issue 8, 2017. 1366…”
Section: Histopathological Examinationmentioning
confidence: 99%