Membrane stabilizing, anti-oxidative interactions of propranolol and dexpropranolol with neutrophils

Anderson, Ronald; Ramafi, Grace; Theron, Annette J.

doi:10.1016/0006-2952(96)00212-2

Cited by 36 publications

(18 citation statements)

References 24 publications

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“…CPU86017 suppresses VF by normalizing an increase in inflammatory factors, which include an excess of ROS, activation of the ET pathway, enhanced iNOS activity and expression, and upregulation of TGF-b expression. We also found that propranolol, a b-receptor blocker, decreases susceptibility to VF, relating to its suppression of antioxidant activity (Anderson et al 1996) and other pro-inflammatory factors that lead to abnormal expression of ERG protein in the myocardium. This is consistent with previous reports that propranolol can be used to treat LQTS (Bar-Cohen & Silka 2006;Hobbs et al 2006).…”

Section: Over-expression Of Erg Proteinmentioning

confidence: 64%

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Dai

et al. 2008

Journal of Pharmacy and Pharmacology

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The aim of this study was to verify whether exaggerated arrhythmogenesis is attributed to inflammatory factors actively involving an excess of reactive oxygen species (ROS), transforming growth factor (TGF)-b and endothelin (ET). We hypothesized that CPU86017, derived from berberine, which possesses multi-channel blocking activity, could suppress inflammatory factors, resulting in inhibition of over-expression of ether-a-go-go (ERG) and an augmented incidence of ventricular fibrillation (VF) in ischaemia/reperfusion (I/R). Rats with cardiomyopathy (CMP) induced by thyroxine (0.2 mg −1 kg −1 s.c. daily for 10 days) were treated with propranolol (10 mgkg −1 p.o.) or CPU86017(80 mgkg −1 p.o.) on days 6-10. On the 11th day, arrhythmogenesis of the CMP was evaluated by I/R.In the CMP control group, an increase in VF incidence was found with the I/R episode, accompanied by increased ROS, which manifested as an increased level of malondialdehyde and decreased activities of SOD, glutathione peroxidase and catalase in the myocardium. Levels of inducible nitric oxide synthase and TGF-b mRNA were increased in association with upregulation of preproET-1 and ETconverting enzyme. We found increased levels of ERG, which correlated well with arrhythmogenesis. Treatment with CPU86017 or propranolol reversed these changes. These experiments verified our hypothesis that the inflammatory factors ROS, iNOS, TGF-b and ET-1 are actively involved in upregulation of ERG and arrhythmogenesis. CPU86017 and propranolol reduced VF by suppressing these inflammatory factors in the myocardium.

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Section: Over-expression Of Erg Proteinmentioning

confidence: 64%

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Dai

et al. 2008

Journal of Pharmacy and Pharmacology

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“…It has been reported that propranolol protects erythrocytes from damage induced by bioactive phospholipids or hypotonic solution via a membrane-stabilizing action. 7) Membrane stabilization decreases membrane fluidity as well as permeability. 12) Because propranolol possesses a membrane stablizing action correlated with a high lipophilicity, 13) it is possible that the high lipophilic properties of ACE inhibitors may play a role in the protection against hemolysis induced by LPC.…”

Section: Discussionmentioning

confidence: 99%

“…Human erythrocytes lack b-aderenoreceptors, 6) ACE-activity, and angiotensin II receptors. Propranolol was used as a reference drug based on established data 7) ; propranolol is known to attenuate LPC-induced hemolysis by a nonspecific mechanism that is different from b-aderenoceptor antagonism. LPC was dissolved in distilled water to achieve the desired concentrations and then allowed to stand at 4°C for at least 12 h. Quinaprilat was dissolved in 0.01 N NaOH and then further diluted with distilled water so that the final concentration of NaOH would be 2-200 mM.…”

mentioning

confidence: 99%

Protective Effects of Quinaprilat and Trandolaprilat, Active Metabolites of Quinapril and Trandolapril, on Hemolysis Induced by Lysophosphatidylcholine in Human Erythrocytes

Hayase

Satomi

Hara

et al. 2003

Biological & Pharmaceutical Bulletin

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We examined the effects of the angiotensin converting enzyme (ACE) inhibitors captopril, enalaprilat, quinapril, and trandolapril, and their active metabolites quinaprilat and trandolaprilat, on hemolysis induced by lysophosphatidylcholine (LPC) in human erythrocytes. LPC induced hemolysis at the concentrations above the critical micelle concentration (4 m mM). Propranolol, used as a reference drug, attenuated the 50% hemolysis induced by 6 m mM LPC at concentrations ranging from 100 nM to 100 m mM. Similarly, quinaprilat (10 m mM) and trandolaprilat (10, 100 m mM) significantly attenuated the LPC-induced hemolysis, but other ACE inhibitors did not. Since propranolol possesses a membrane stabilizing action correlated with high lipophilicity, it appears that the high lipophilicity of quinaprilat or trandolaprilat is responsible for the protection from the damage induced by LPC. However, quinapril and trandolapril were not effective, although both drugs have higher lipophilicity than quinaprilat and trandolaprilat. Hence, it is suggested that the high lipophilicity alone may not contribute to the protective effects of ACE inhibitors against LPC-induced hemolysis. None of ACE inhibitors attenuated the hypotonic hemolysis (60 mM NaCl), although propranolol did. Furthermore, neither propranolol (100 m mM) nor quinaprilat (50 m mM) and trandolaprilat (50 m mM) affected LPC micelle formation, suggesting that these drugs do not directly bind to LPC. We therefore believe that the protective effects of quinaprilat and trandolaprilat on the LPC-induced hemolysis may be related physicochemically to their highly lipophilic and ACE inhibitory structures, which probably maintain erythrocyte membrane integrity by a mechanism other than ACE inhibition, prevention of LPC micelle formation or protection against osmotic imbalance.

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“…Thereby, it can also result in the central inhibition of the sympathetic nervous system. The unique stability effect on the membrane of myocytes has also been described (4). Previous studies showed that propranolol in combination with amiodarone offered the best prevention of VT relapses (5).…”

mentioning

confidence: 92%

Propranolol efficiency in prevention of sustained ventricular tachycardia in patients with implanted cardioverter-defibrillator: a case series

Puljević¹,

Velagić²,

Puljević³

et al. 2014

Croat Med J

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Membrane stabilizing, anti-oxidative interactions of propranolol and dexpropranolol with neutrophils

Cited by 36 publications

References 24 publications

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Protective Effects of Quinaprilat and Trandolaprilat, Active Metabolites of Quinapril and Trandolapril, on Hemolysis Induced by Lysophosphatidylcholine in Human Erythrocytes

Propranolol efficiency in prevention of sustained ventricular tachycardia in patients with implanted cardioverter-defibrillator: a case series

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