Abstract
The cognitive function of brain and contractility of heart muscle are accompanied with age-dependent dehydration of tissues of these two organs. The aim of the present study is to reveal which of the abovementioned two organs primarily fail as a result of dysfunction of age-sensitive metabolic mechanism. For this purpose, the age-dependent sensitivity of cell hydration in brain cortex and heart muscle tissues are studied through depressing metabolic activity by cooling and its activation by supplying animals with distilled water, by inactivation of Na+/K+ pump and activation of Na+/Ca2+ exchange in the reverse mode. The obtained data bring us to the conclusion that the metabolic regulation of brain cortex and heart muscle tissues has different nature. The age-dependent dysfunction of Na+/K+ pump–induced activation of RNa+/Ca2+ exchange leads to dysfunction of heart muscle contractility because of activation of Ca-calmoduline-NO-cGMP production, which brings to FNa+/Ca2+ exchange induced muscle relaxation and it could serve as a primary mechanism for dysfunction of brain tissues’ metabolic control of cell hydration, which leads to overexpression of Na+/Ca2+ exchanger in the membrane.
Highlights
The dysfunction of metabolic controlling of cell hydration is a common consequence of any cell pathology, including aging
[3H]-ouabain leads to age-dependent increase of hydration in brain cortex tissues, which is accompanied with agedependent decrease of the number of [3H]-ouabain bound molecules with cell membrane (Figure 2C, E)
Our previous study has shown that in living cells the metabolic driving of water efflux from the cells is a key regulating the cell membrane excitability, which is realized by direct inactivation of inward ionic currents, such as Na+ and Ca2+ currents, through the membrane and surfacedependent decrease of functional active ionic channels in the membrane [1, 3]
Summary
The dysfunction of metabolic controlling of cell hydration is a common consequence of any cell pathology, including aging. It is known that aging-induced impairments of cognitive function of brain and contractility of heart muscle are accompanied with dehydration of tissues of these two organs. Which of the abovementioned two organs primarily fail as a result of dysfunction of age-sensitive metabolic mechanism is not clear yet. The metabolic driving of water efflux from the cell, having inhibitory effect on inward ionic currents such as INa and ICa [3], serves as a key metabolic mechanism controlling low permeability of cell membrane (membrane excitability) for these ions [6].
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