Triphosphoric Acid, Donated, Restores Heart Rhythm Disturbances Caused by Energetically Deficient, Mitochondrial Hypercalcaemia to Ca++ Mpt Pore Lesion

Abstract

Ca ++ mPT pore damage leads to ↑ Ca ++ in the mitochondria (M), where Ca ++ pumps ↓H + and ↑pH, through the disordered depolarization ↓electric potential of the internal M membrane, ATP synthesis is also afect, which is manifested by a mitochondrial energy deficit (MED). MED provoke→ cell hypo -anergy→oxidative stress, OS→ collapse M→M swells → osmotic demyelination→membrane rupture M→detritus mass output with large molecule in intermembrane space M→in cell cytosol→apoptosis-inducing factor→cytochrome C→which are the predictors of programmed cell death. Contributing to the increase in blood pressure to OS not only hyperadrenalinemia, but also the reduction of the effect of vasorelaxation by NO, which ↓ as it becomes becomes a trap for the excess oxygen free radicals, especially for oxygen superoxide. Triphosphoric acid (ATP), donated, as an energetic carrier, mitochondrial permeability transition pore-dependent Ca++uniporter, mPT pore, restores the disorder of electrical cardiac potentials: ↓Conductivity, ↑refractoriness of the atrioventricular node, ↓sinus nodule automatism, and primary hypertension, caused by MED and, further, manifested by the microcirculatory and mitochondrial distress syndrome. Simultaneously, ATP influences: Mitochondrial ATP-dependent potassium channel, mitoKATP; acetylcholinedependent potassium channel, KACh cholinergic-M receptor; receptors: Adenosine A1; and purine P2. M myocardial cells create mesh nets that limit the disordered energy flow in the reduced M space, avoiding damage to the entire heart muscle. As a result, M also plays the role of the electroconductivity switch, which protects the heart from the extent of the damage of a "short circuit" in area necrotizing myocardiocytes and M hypoanergic. Hence, the anti-arrhythmogenic effect of ATP-energetic

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“…Inflammatory during SARS-CoV-2 infection is dependent on Ca2+ level. The process is determined by the opening/closing of the mitochondrial permeability transition pore-dependent Ca++uniporter (mPT pore), which we have described sufficiently in the Universal Medical Journal [59,60].…”

Lipid Therapy for Dyslipidemic Disorders Activates 21st Century Nano Antioxidant Hydrogen as a Potential Anti-COVID-19 Agent: Review

“…[33,34]. Described disrupting the opening / closing of the Mitochondrial permeability transition pore-dependent Ca 2+ uniporter, mPT pore [29,35]. Coinciding with destruction of lipid rafts that stops the movement of Ca 2+ waves in cells and calcium ion surges modify functions of normal and pathologically altered cells, such as proliferation, maintenance of life, apoptosis and necrosis.…”

“…Depending on the disorders of the element's hydrogen, carbon and oxygen atoms, as well as phosphorus, sulfur, nitrogen and other elements that determine cellular function. Disorder of oxygen and nitrogen in the form of Oxidative and Nitro-Galogenic Stress in Patients with SARS-Cov2 / COVID / 19 when generating Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) is described [29], phosphorus, as ATP energy carrier [35,39]. Now examine the role of hydrogen.…”