Interaction of intracellular electrolytes and tubular transport.
To disclose possible regulatory mechanisms, the potential difference across the peritubular cell membrane (PDpt) and intracellular activities of sodium (Nai+), potassium (Ki+), calcium (Cai2+), bicarbonate (HCO3i-) and chloride (Cli-) have been traced continuously during inhibition of Na+/K+-ATPase with ouabain. Within 31 +/- 4 min following application of ouabain, PDpt decreases (from 57 +/- 2 mV) to half and Ki+ by 37.7 +/- 2.2 mmol/l (from 63.5 +/- 1.9 mmol/l), Nai+ increases by 35.1 +/- 4.1 mmol/l (from 13.2 +/- 2.4 mmol/l), Cai2+ by 0.17 +/- 0.2 mumol/l (from 0.09 mumol/l), HCO3i-) by 3.0 +/- 1.1 mmol/l (from 15.3 +/- 2.0 mmol/l) and Cli- by 6.2 +/- 1.0 mmol/l (from 14.4 +/- 1.6 mmol/l). Within the same time the luminal and peritubular cell membrane resistances increase 45 +/- 15% and 53 +/- 17%, respectively. The increase of the resistances is mainly due to a decrease of K+ conductance, which in turn mainly accounts for the depolarisation of PDpt. Additional experiments demonstrate that the K+ conductance of the peritubular cell membrane is sensitive to the cell membrane potential difference and possibly linked to Na+/K+-ATPase activity. The decline of PDpt probably accounts for intracellular alkalinisation which in turn reduces Na+/H+ exchange. Na+-coupled transport of glucose and phenylalanine decrease in linear proportion to PDpt. The transport of these and probably of similar substances represents the main threat to electrolyte homeostasis of the cells.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D002462:Cell Membrane; D004566:Electrodes; D004573:Electrolytes / Q000378:metabolism*; D006801:Humans; D007684:Kidney Tubules / Q000201:enzymology / Q000378:metabolism*; D008564:Membrane Potentials; D010042:Ouabain / Q000494:pharmacology
D004573:Electrolytes; D010042:Ouabain; D000251:Adenosine Triphosphatases