Sodium permeability and myocardial resistance to cell swelling during metabolic blockade

Abstract

The role of cell membrane permeability to sodium in cell volume regulation during inhibition of the sodium-potassium exchange pump with ouabain and during total metabolic blockade was evaluated in sections of guinea pig renal cortex, ventricle, and atrium incubated in Krebs-Henseleit solution. In all tissues, 2 and 3 h of ouabain and metabolic blockade resulted in similar marked losses of potassium and parallel continuous reductions in resting membrane potentials. Only metabolic blockade of renal cortex increased cell water, chloride, and total monovalent cations (potassium plus sodium) significantly. Compared to ouabain, metabolic blockade markedly increased the rate of cellular washout of 24Na+ from renal cortex (t 1/2 reduced by 47%), which was significantly greater than reductions in t 1/2 from ventricle (16%) and atrium (15%). Thus, inhibition of sodium-potassium exchange pump activity was not sufficient to produce cell swelling unless associated with marked increases in cell membrane permeability to sodium, in which case sodium influx exceeded potassium loss and substantial increases in monovalent cations, chloride, and water occurred.

Role of Ca2+ Transporters and Channels in the Cardiac Cell Volume Regulation

“…In experiments, the treatment with 40 μM ouabain caused membrane depolarization (Δ V m = 51.7 ± 4.3 mV from resting V m of –91.7 ± 6.4 mV). In contrast to V m , no obvious cell swelling was observed (the cell area at 90 min was 96.9 ± 0.7% of the original area), which was in agreement with the previous reports 4,5 . The Kyoto model well simulates the time course of membrane depolarization and almost constant cell volume during the ouabain exposure (.…”

“…Interestingly, it is well known that the cardiac cell volume hardly changes during the Na + /K + pump blockade 4,5 . Taken the above theoretical mechanisms into consideration, the cell volume maintenance in the cardiac myocytes may be partially explained by the low‐membrane Na + and Cl − permeabilities in these cells.…”

“…It also depends on the membrane Na + permeability indirectly through affecting the redistribution of K + across the membrane and V m. 3 Interestingly, it is well known that the cardiac cell volume hardly changes during the Na + /K + pump blockade. 4,5 Taken the above theoretical mechanisms into consideration, the cell volume maintenance in the cardiac myocytes may be partially explained by the low-membrane Na + and Cl − permeabilities in these cells. However, role of Ca 2+ , which should increase during the Na + /K + pump blockade, in the cell volume regulation has not been well clarified.…”

Intracellular Volume Measurement and Detection of Edema: Multinuclear NMR Studies of Intact Rat Hearts during Normothermic Ischemia

“…The apex was cut and the excess of water was absorbed by filter paper for 1 min, and the wet weight determined. Both parts of the heart were dried for 24 h at 80°C to determine the dry weights.…”

Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

“…These changes may form the basis for an increase in the intracellular osmotic pressure and water entry into the cytoplasm [1,5,11]. It is supposed that extreme cardiomyocyte swelling may be a cause of mechanical rupture of the sarcolemma [6,12].…”