Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
K+ balance in mammals relies on regulated renal K+ excretion matching unregulated fluctuating K+ intake. Upon a K+ rich meal, rapid and powerful K+ excretion is needed. Renal K+ secretion is stimulated by the increased tubular flow. We speculated that high K+ intake acutely increases urinary flow to stimulate K+ excretion.
Methods
Mice were K+ challenged through diets or gavage. Post K+ loading urinary output, osmolarity, [K+]u, [Na+]u, plasma osmolarity, [copeptin]p, [K+]p, and [Na+]p were measured. To locate the mechanism of K+‐induced diuresis in the glomerular/tubular system we measured creatinine excretion and assessed functional transport in isolated perfused TALs and CDs during an acute [K+]bl switch from 3.6 to 6.5 mM. Molecular adaptations of transport proteins involved in water reabsorption were investigated by immunoblotting.
Results
(1) Mice switched from a 1% to 2% K+ diet increased diuresis within 12 hours and reciprocally reduced diuresis when switched from 1% to 0.01% K+ diet. (2) A single K+ gavage load, corresponding to 25%‐50% of daily K+ intake, induced 100% increase in diuresis within 30 minutes. This occurred despite augmented plasma osmolarity and AVP synthesis. (3) K+ gavage did not change GFR. (4) In isolated perfused TALs, shifting [K+]bl from 3.6 to 6.5 mM did not affect AVP‐induced NaCl transport. (5) In sharp contrast, in isolated perfused CDs, shifting [K+]bl from 3.6 to 6.5 mM markedly reduced CD AVP sensitivity, ie inhibited water absorption.
Conclusion
Dietary K+ loading induces a rapidly on‐setting diuresis. The mechanism of K+‐induced diuresis involves desensitization of the CD to AVP.