No abstract

The Malvin, Sullivan and Wilde ( The Physiologist 1: 58, 1957) stop flow technique for the localization of tubular function has been applied to a study of potassium and acid excretion in the dog. It has been observed that the urine is acidified in the distal part of the nephron at a site of avid sodium reabsorption. Potassium and ammonia are secreted in the same portion of the tubule. Diamox reduces acidification of the urine and secretion of ammonia and enhances the secretion of potassium. Phosphate is reabsorbed in the proximal part of the nephron in a region which is coextensive with that which secretes p-aminohippurate. All our data are consonant with the view that a mechanism located in the distal part of the nephron exchanges cellular hydrogen and/or potassium ions for sodium ions in the tubular urine. Ammonia diffuses into acid urine and is trapped as ammonium ion. Diamox, by interfering with the supply of cellular hydrogen ions, reduces exchange of hydrogen for sodium and favors the exchange of potassium for sodium.

We have used in vitro techniques to study the metabolism of dexamethasone. Tissue slices, homogenates and microsomal fractions of various mammalian organs from rats and humans have been used. We focused particularly on the question of whether or not dexamethasone (Dexa) is oxidized at the C11-OH group by 11β-hydroxysteroid-dehydrogenase. High activities of this enzyme system for Dexa were localized in renal cortex and rectum. Material from both human and murine liver was ineffective. The main metabolite formed from Dexa in renal and intestinal systems was identified by different mass-spectrometric techniques including on line HPLC mass spectrometry as 11-dehydro-dexamethasone. This finding was corroborated by the observation that both corticosterone and glycyrrhetinic acid block the metabolic transformation of Dexa.