title: Electrophysiology of rat distal colon after partial nephrectomy. Implications for K transport.
abstract: Previous in vivo studies in rat and man indicate that chronic renal insufficiency leads to an increase in the capacity of the large intestine for K secretion. The present studies were performed in isolated rat distal colon with conventional and K-sensitive microelectrodes to determine the cellular basis for enhanced colonic K secretion after 70% nephrectomy. The data revealed that in animals fed a regular diet, nephrectomy had no effect on the Na or K conductance of the apical membrane, or the kinetics of the basolateral membrane Na-K pump, but intracellular K activity decreased from 70 +/- 4 mmol/l to 58 +/- 4 mmol/l (P less than 0.005). In control (non-nephrectomised) animals, feeding a diet modestly (4-fold) enriched with K resulted in small but significant increases in the Na and K conductance of the apical membrane, no change in the kinetics of the basolateral membrane Na-K pump, and a rise in intracellular K activity from 70 +/- 4 mmol/l to 94 +/- 7 mmol/l (P less than 0.005). In contrast, in animals fed the K enriched diet, nephrectomy resulted in (i) large, amiloride-sensitive increases in transepithelial voltage and total tissue conductance (consistent with an appreciable degree of secondary hyperaldosteronism), (ii) marked increases in the Na and K conductance of the apical membrane, (iii) significant hyperpolarization of the basolateral membrane, (iv) a 100% increase (P less than 0.02) in the maximum activity of the basolateral membrane Na-K pump, and (v) a rise in intracellular K activity from 94 +/- 7 mmol/l to 129 +/- 7 mmol/l (P less than 0.0025). These data suggest that the combination of modest dietary K enrichment and 70% nephrectomy stimulated an active K secretory process which reflected an increase in the K excretory load applied to the colonic mucosa, and the effects of aldosterone. In this model of renal insufficiency, enhanced K secretion by the transcellular and paracellular (potential-dependent) pathways results in a marked rise in the K excretory capacity of the colon.
authors.affiliation: Department of Medicine, Hope Hospital (University of Manchester School of Medicine), Salford, Great Britain.
authors.forename: G I
authors.initials: GI
authors.lastname: Sandle
authors.forename: F
authors.initials: F
authors.lastname: McGlone
authors.forename: R J
authors.initials: RJ
authors.lastname: Davies
mesh_terms: D000818:Animals; D001692:Biological Transport; D003106:Colon / Q000502:physiology*; D004032:Diet; D004553:Electric Conductivity; D004594:Electrophysiology; D007668:Kidney / Q000503:physiopathology; D008297:Male; D009392:Nephrectomy; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000502:physiology
chemical_list: D012964:Sodium; D011188:Potassium