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Abstract

Using the stop flow microperfusion technique with simultaneous capillary perfusion the secretory rate of H⁺ ions in the proximal tubule was evaluated by measuring the level flow reabsorption as well as the static head concentration difference of ³H labeled glycodiazine. At ambient glycodiazine concentration of 21 mmol/l the level flow reabsorption is in the same range as that of bicarbonate. In the early proximal loops the reabsorption is 20% greater than in the late proximal loops. The carbonic anhydrase inhibitors acetazolamide and 3,4-methylene-dioxyphenyl-sulfonamide (both 10^-4 M) as well as furosemide (10^-3 M) inhibit the glycodiazine reabsorption 43%, 27% and 22% respectively. Thiocyanate (2-10^-2 M), however, exerted only an insignificant inhibition (12%). When Na⁺ in the ambient perfusion solutions was replaced by Li⁺ or choline⁺ the glycodiazine transport was strongly reduced. Ouabain (5-10^-2 M) inhibited too, but amiloride (10^-3 M) had no effect on glycodiazine transport. The glycodiazine transport was 28% reduced in metabolic alkalosis and to a smaller although significant extent (17%) in metabolic acidosis; it was unchanged in chronic hypercapnia. In chronic K⁺ depletion the glycodiazine reabsorption was accelerated by 12% only in the early proximal loops. Chronic parathyroidectomy as well as acute substitution with parathyroid hormone had no effect on the glycodiazine absorption. The main conclusions are: Proximal H⁺ transport proceeds with suitable buffers. Although independent of HCO₃^- and carbonic anhydrase, it could be partially inhibited by CA inhibitors. H⁺ transport is supposed to proceed as countertransport with Na⁺ ions. In chronic alkalosis the H⁺ transport is reduced.