Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Peineau, Nicolas; Mongo, K.G.; Guennec, J.-Y. Le; Garnier, D; Argibay, Jorge

doi:10.1111/j.1476-5381.1992.tb14470.x

Cited by 3 publications

(5 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among the top 10 compounds, trichostatin A (Figure 4B) and heptaminol (Figure 4C) had the highest binding affinity to CDK1, which was mutually confirmed by previous studies [48]. Furthermore, heptaminol has been proven to treat cardiovascular system problems such as anti-hypotensive action, right heart failure, and cardiogenic edema [49,50], therefore it was selected as the key drug.…”

Section: Correlation Between Cdk1 and Compounds Via Molecular Dockingsupporting

confidence: 65%

“…The chemical structures of these compounds were also downloaded (Figure 4A) from the ZINC database (http://zinc15.docking.org). Among these small compounds, previous studies have proven that heptaminol [44,45] and tranexamic acid [46] can be used in cardiovascular diseases, while the others have the effects of anti-tumor or antiinflammatory, etc.…”

Section: Candidate Anti-cardiotoxicity Compounds Via Cmap Analysismentioning

confidence: 99%

“…Meanwhile, our study also found that cardiac injury induced by AC exposure in zebrafish mainly included pericardial edema and atrial enlargement. Heptaminol was widely recognized for the treatment for right heart failure, coronary heart disease, and cardiogenic edema, which can improve atrioventricular node excitability, excite the conduction system, and restore its normal function [44,45,64].…”

Section: E924092-10mentioning

confidence: 99%

See 2 more Smart Citations

Potential Molecular Mechanisms and Drugs for Aconitine-Induced Cardiotoxicity in Zebrafish through RNA Sequencing and Bioinformatics Analysis

et al. 2020

View full text Add to dashboard Cite

Background:Accumulating evidence suggests that cardiotoxicity is one of the main manifestations of aconitine (AC) poisoning. However, the molecular mechanism of AC-induced cardiotoxicity remains unclear, there is little direct evidence for therapeutic targets and drugs of AC-induced cardiotoxicity. Material/Methods:Zebrafish were exposed to AC to evaluate cardiotoxicity by calculating the heart rates and observing the changes of cardiac and vascular structure. RNA-seq (RNA sequencing) and bioinformatics analysis were used to obtain differentially expressed genes (DEGs). The anti-AC cardiotoxicity compound was identified via connectivity map (CMAP) analysis and molecular docking. Results:AC-induced cardiotoxicity in zebrafish predominantly included arrhythmias, extended sinus venous and bulbus arteriosus (SV-BA) distance, and larger pericardial edema aera. A total of 1380 DEGs were identified by RNA-seq and bioinformatics analysis. cyclin-dependent kinase-1 (CDK1) was screened as the hub gene and the most potential therapeutic target due to its significant downregulation in cardiotoxicity based on protein-protein interaction (PPI) and drug-gene interaction (DGIdb) network analysis. Cell cycle signal pathway was the most significant pathways identified in the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Furthermore, the expression of CDK1 was validated in the Gene Expression Omnibus (GEO) database GSE71906, GSE65705, and GSE95140. Finally, heptaminol was identified as a novel anti-AC cardiotoxicity compound via CMAP analysis and molecular docking. Conclusions:Totally, hub genes and key pathways identified in this study can aid in the understanding of the molecular changes in AC-induced cardiotoxicity. Meanwhile, we provide a systematic method to explore drug toxicity prevention and treatment.

show abstract

Section: Correlation Between Cdk1 and Compounds Via Molecular Dockingsupporting

confidence: 65%

Section: Candidate Anti-cardiotoxicity Compounds Via Cmap Analysismentioning

confidence: 99%

Section: E924092-10mentioning

confidence: 99%

See 1 more Smart Citation

Potential Molecular Mechanisms and Drugs for Aconitine-Induced Cardiotoxicity in Zebrafish through RNA Sequencing and Bioinformatics Analysis

et al. 2020

View full text Add to dashboard Cite

show abstract

“…It has been used to treat low blood pressure and orthostatic hypotension ( Boismare and Boquet, 1975 ), with reported ‘unexpected’ adverse effects ( Pathak et al ., 2005 ). Its actions may involve NA release by action at the transporter ( Grobecker and Grobecker, 1976 ; Delicado et al ., 1990 ), but it may also have effects on Ca2+ channels to increase intracellular calcium ( Peineau et al ., 1992 ). See also Isometheptene.…”

Section: Compounds Listed By Mode Of Actionmentioning

confidence: 99%

Pharmacology of stimulants prohibited by the World Anti‐Doping Agency (WADA)

Docherty

2008

British J Pharmacology

110

View full text Add to dashboard Cite

This review examines the pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA). Stimulants that increase alertness/reduce fatigue or activate the cardiovascular system can include drugs like ephedrine available in many overthe-counter medicines. Others such as amphetamines, cocaine and hallucinogenic drugs, available on prescription or illegally, can modify mood. A total of 62 stimulants (61 chemical entities) are listed in the WADA List, prohibited in competition. Athletes may have stimulants in their body for one of three main reasons: inadvertent consumption in a propriety medicine; deliberate consumption for misuse as a recreational drug and deliberate consumption to enhance performance. The majority of stimulants on the list act on the monoaminergic systems: adrenergic (sympathetic, transmitter noradrenaline), dopaminergic (transmitter dopamine) and serotonergic (transmitter serotonin, 5-HT). Sympathomimetic describes agents, which mimic sympathetic responses, and dopaminomimetic and serotoninomimetic can be used to describe actions on the dopamine and serotonin systems. However, many agents act to mimic more than one of these monoamines, so that a collective term of monoaminomimetic may be useful. Monoaminomimietic actions of stimulants can include blockade of re-uptake of neurotransmitter, indirect release of neurotransmitter, direct activation of monoaminergic receptors. Many of the stimulants are amphetamines or amphetamine derivatives, including agents with abuse potential as recreational drugs. A number of agents are metabolized to amphetamine or metamphetamine. In addition to the monoaminomimetic agents, a small number of agents with different modes of action are on the list. A number of commonly used stimulants are not considered as Prohibited Substances.

show abstract

“…Pindolol was chosen over carvedilol for current study due to its lack of α-adrenoreceptor blocking activity. Heptaminol, on the other hand, is a vasodilator and a general antagonist to catecholamine release and uptake that also raises intracellular free calcium level [12, 13]. Lastly verapamil is an L-type calcium channel blocker.…”

Section: Introductionmentioning

confidence: 99%

NO-dependent attenuation of TPA-induced immunoinflammatory skin changes in Balb/c mice by pindolol, heptaminol or ATRA, but not by verapamil

Chung¹,

Yoon

Cheon

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Recently a mouse skin carcinogenesis study reported that a β-blocker carvedilol displayed antitumor-properties via antihyperplastic effects. However, the antihyperplastic mechanism is unclear as the β-blocker is characterized with multiple pleiotropic effects including stimulation of endothelial NO release and verapamil-like calcium channel blocking activity. To investigate the nature and the origin of the antihyperplastic effects, we tested topical pretreatment with pindolol, heptaminol, ATRA or verapamil against Balb/c mouse ear skin hyperplasia that was induced by TPA. We found that pindolol, heptaminol or ATRA, but not verapamil, inhibited the TPA-induced immunoinflammatory skin changes in an NO-dependent manner, which included epidermal hyperplasia, skin edema and fibrosis. Furthermore, we also observed NO-dependent alleviation of the TPA-induced NK cell depletion in the ear tissues by heptaminol pretreatment. Together our results suggest that stimulation of NO generation from constitutive synthases may be primarily responsible for the reported antihyperplastic and NK cell-preserving effects of the β-blockers, and that similar effects may be observed in other immunity normalizing compounds that also promote endothelial NO synthesis.

show abstract

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Cited by 3 publications

References 37 publications

Potential Molecular Mechanisms and Drugs for Aconitine-Induced Cardiotoxicity in Zebrafish through RNA Sequencing and Bioinformatics Analysis

Potential Molecular Mechanisms and Drugs for Aconitine-Induced Cardiotoxicity in Zebrafish through RNA Sequencing and Bioinformatics Analysis

Pharmacology of stimulants prohibited by the World Anti‐Doping Agency (WADA)

NO-dependent attenuation of TPA-induced immunoinflammatory skin changes in Balb/c mice by pindolol, heptaminol or ATRA, but not by verapamil

Contact Info

Product

Resources

About