Amlodipine: The double edged sword

Rabah, Fatma; El-Naggari, Mohamed; Al-Nabhani, Dana

doi:10.1111/jpc.13517

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…by the prolongation of action and a higher safety profile [163,164]. Drugs of this group have a cardioprotective effect by improving myocardial perfusion, reducing myocardial oxygen demand, and reducing the formation of free radicals and mitochondrial Ca 2+ overloading of CM [163][164][165]. The disadvantages of CCBs as drugs are their rather wide range of action and low selectivity with respect to their molecular targets directly in the myocardium.…”

Section: Prospects Of Using the Achievements Of Molecular Biology In ...mentioning

confidence: 99%

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Shemarova

2023

IJMS

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Chronic heart diseases, such as coronary heart disease, heart failure, secondary arterial hypertension, and dilated and hypertrophic cardiomyopathies, are widespread and have a fairly high incidence of mortality and disability. Most of these diseases are characterized by cardiac arrhythmias, conduction, and contractility disorders. Additionally, interruption of the electrical activity of the heart, the appearance of extensive ectopic foci, and heart failure are all symptoms of a number of severe hereditary diseases. The molecular mechanisms leading to the development of heart diseases are associated with impaired permeability and excitability of cell membranes and are mainly caused by the dysfunction of cardiac Ca2+ channels. Over the past 50 years, more than 100 varieties of ion channels have been found in the cardiovascular cells. The relationship between the activity of these channels and cardiac pathology, as well as the general cellular biological function, has been intensively studied on several cell types and experimental animal models in vivo and in situ. In this review, I discuss the origin of genetic Ca2+ channelopathies of L- and T-type voltage-gated calcium channels in humans and the role of the non-genetic dysfunctions of Ca2+ channels of various types: L-, R-, and T-type voltage-gated calcium channels, RyR2, including Ca2+ permeable nonselective cation hyperpolarization-activated cyclic nucleotide-gated (HCN), and transient receptor potential (TRP) channels, in the development of cardiac pathology in humans, as well as various aspects of promising experimental studies of the dysfunctions of these channels performed on animal models or in vitro.

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Section: Prospects Of Using the Achievements Of Molecular Biology In ...mentioning

confidence: 99%

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Shemarova

2023

IJMS

View full text Add to dashboard Cite

show abstract

“…by prolongation of action, and a higher safety profile [164,165]. Drugs of this group have a cardioprotective effect by improving myocardial perfusion, reducing myocardial oxygen demand, reducing the formation of free radicals and mitochondrial Ca2+ overloading of CM [164][165][166]. The disadvantages of CCBs as drugs are their rather wide range of action and low selectivity with respect to their molecular targets directly in the myocardium.…”

Section: Prospects Of Using the Achievements Of Molecular Biology In ...mentioning

confidence: 99%

Dysfunction of Ca2+ Channels in Hereditary and Chronic Cardiovascular Diseases

Шемарова¹

2023

Preprint

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Cardiovascular diseases (CVD) account for about 17.3 million annual deaths worldwide. 85% of these deaths occurred as a result of myocardial infarction (MI) and stroke. Chronic heart diseases, such as arterial hypertension (AH), coronary heart disease, various cerebrovascular diseases, dilated and hypertrophic cardiomyopathies are widespread, with a fairly high incidence of mortality and disability. Most of these diseases are characterized by cardiac arrhythmias, conduction and contractility disorders. Additionally, interruption of the electrical activity of the heart, the appearance of extensive ectopic foci and heart failure are all symptoms of a number of severe hereditary diseases. The molecular mechanisms leading to the development of CVD are associated with impaired permeability and excitability of cell membranes and mainly caused by dysfunction of cardiac Ca2+ channels. Acquired channelopathies are caused by metabolic disorders, increased tone of the sympathetic nervous system, age-related changes that lead to deterioration of coronary blood flow and hemodynamics. Currently known channelopathies, such as the long or short QT syndromes, Brugada and Lenegre syndromes, catecholaminergic polymorphic ventricular tachycardia, etc., are congenital and genetic disorders caused by mutations of genes "responsible" for the conductive properties of certain channel-forming proteins, including pore-forming subunits of Ca2+ channels. Over the past 50 years, more than 100 varieties of ion channels have been found in the cardiovascular system cells. The relationship between the activity of these channels and cardiac pathology, as well as the general cellular biological function, has been intensively studied on several cell types and experimental animal models in vivo и in situ. In this review, we discuss the origin of Ca2+ channelopathies and the role of Ca2+ channels of various types: L- R-, T-types voltage-gated calcium channels, RyR2, non-selective hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, transient receptor potential (TRPC, TRPM7, TRPA1) channels in the development of cardio-vascular pathology.

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“…It has the functions of enhancing blood flow, lowering blood pressure, long-acting time, slow-onset [4,5]. If such prescription drugs are not used as required, they may cause electrolytes in the human body to flocculate, resulting in metabolic abnormalities, hyponatremia, hypokalemia, peripheral edema, and other side effects [6]. At present, the methods commonly used to detect the content of AB include reversed-phase ultrahigh performance liquid chromatography-mass spectrometry [7], liquid chromatography-tandem mass spectrometry [8], electrochemical [9], spectrophotometry [10,11], and fluorescence spectroscopy [12].…”

Section: Introductionmentioning

confidence: 99%

A Photoelectrochemical Sensor for Firstly the Detection of Amlodipine Besylate Based on an MnC₄Pc Coated ZnO Composite Materials

Shao

2022

Electroanalysis

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In this study, tetracarboxylic manganese phthalocyanine coated nano-zinc oxide (MnC 4 Pc-ZnO) composite material was prepared by in-situ growth method and modified with indium tin oxide (ITO) glass electrode to construct a photoelectrochemical (PEC) sensor. A PEC sensor for the determination of amlodipine besylate (AB) was developed for the first time based on the principle of precipitation reaction between heavy metal ions and dihydropyridine and the recombination suppression effect of the material. The morphology and optical properties of the MnC 4 Pc-ZnO composites were characterized by scanning electron microscopy (SEM) and ultravioletvisible diffuse reflectance spectroscopy (UV-vis DRS). Chronoamperometry (i-t) and electrochemical impedance spectroscopy (EIS) were used to study the PEC behavior of ITO electrodes modified by MnC 4 Pc-ZnO composite material. The study found that the MnC 4 Pc-ZnO composite material has a good photocurrent response to AB, and there was a good linear relationship between the concentration range of 75 nM-250 μM, the linear equation was I(μA) = À 5.2 × 10 À 8 × lgC + 3.2 × 10 À 8 (r = 0.9947), a limit of detection (LOD) of 20 nM. In addition, MnC 4 Pc-ZnO/ITO also has good selectivity and stability. The PEC sensor detects amlodipine besylate tablets, amlodipine besylate dispersible tablets, and biological samples, with standard addition recovery rates of 96.11 % and 103.96 %, respectively. The determination result has good accuracy, and the PEC sensor provides a new method for detecting AB.

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Amlodipine: The double edged sword

Abstract: Resolution of the oedema with stoppage of amlodipine confirms its culprit as a cause of the oedema. To our knowledge, this is the largest case series of amlodipine-related generalised oedema in the paediatric population.

Cited by 7 publications

References 15 publications

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Dysfunction of Ca2+ Channels in Hereditary and Chronic Cardiovascular Diseases

A Photoelectrochemical Sensor for Firstly the Detection of Amlodipine Besylate Based on an MnC₄Pc Coated ZnO Composite Materials

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Amlodipine: The double edged sword

Abstract: Resolution of the oedema with stoppage of amlodipine confirms its culprit as a cause of the oedema. To our knowledge, this is the largest case series of amlodipine-related generalised oedema in the paediatric population.

Cited by 7 publications

References 15 publications

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Dysfunction of Ca2+ Channels in Hereditary and Chronic Cardiovascular Diseases

A Photoelectrochemical Sensor for Firstly the Detection of Amlodipine Besylate Based on an MnC4Pc Coated ZnO Composite Materials

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Product

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A Photoelectrochemical Sensor for Firstly the Detection of Amlodipine Besylate Based on an MnC₄Pc Coated ZnO Composite Materials