[On the etiology of water excretion inhibition in Addison's disease].
Micropuncture experiments, performed on adrenalectomized rats disclosed an impairment of the hypertonic sodium chloride transport of the thick ascending limb of Henle's loop (the diluting segment). This transport inhibition was documented by a delayed time course of NaCl-concentration decrease within the diluting segment. Assuming a pump leak model of the hypertonic NaCl-transport, we calculated a 50% inhibition of the NaCl-transport velocity compared with controls. Dexamethasone treatment for 3 days led to a normalization of the impaired transport velocity. Both, the reduced GFR as well as the impaired free water clearance are functionally linked to the diminished transport capacity of the diluting segment by the tubuloglomerular feedback mechanism and the ADH mechanism respectively. A new hypothesis on the pathogenesis of the water excretion inhibition in adrenal insufficiency is discussed.
D000224:Addison Disease / Q000503:physiopathology*; D000315:Adrenalectomy; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007684:Kidney Tubules / Q000378:metabolism*; D008138:Loop of Henle / Q000378:metabolism*; D008297:Male; D051381:Rats; D012965:Sodium Chloride / Q000378:metabolism*; D014882:Water-Electrolyte Balance
D012965:Sodium Chloride; D003907:Dexamethasone
Zur Atiologie der Wasserausscheidungsstörung bei Morbus Addison.