CHLORIDE SECRETION DRIVES URINE FORMATION IN LEECH NEPHRIDIA

The transport mechanisms underlying urine formation in leech nephridia were investigated in situ and in isolated preparations using pharmaco logical, electrophysiological and micropuncture techniques, Canalicula r cells, which secrete the primary urine, function as a Cl--secreting epithelium. An apical Cl- conductance contributes to the lumen-negativ e potential which drives transcellular K+ transport and paracellular N a+ transport. On the basolateral side, a ouabain-sensitive Na+/K+-ATPa se contributes substantially to the cellular and transcellular potenti al and provides the Na+ gradient necessary for a bumetanide-sensitive Na+/K+/2Cl(-) cotransport. Final urine is formed by subsequent reabsor ption of ions along the central canal, where KCl and NaCl are reabsorb ed in different portions. The postprandial diuresis is not a consequen ce of the changes in blood osmolality or ion concentrations. Similar c hanges in the ionic environment do not promote diuresis in isolated ne phridia. Apparently, the composition and volume of the primary urine c annot be separately controlled, Any increase in fluid secretion by lee ch canalicular cells involves upregulation of the paracellular pathway and stimulation of Cl- entry, which thereby changes the normally K+-e nriched primary urine to the Na+-enriched primary urine characteristic of leeches in diuresis.