KIDNEY AND URINARY BLADDER RESPONSES OF FRESHWATER RAINBOW TROUT TO ISOSMOTIC NaCI AND NaHCO3 INFUSION

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140mmoll~' NaCI or 140mmoll' NaHCCb (3 ml kg" 'h" 1 ) for 32 h. NaCI had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCCh"] and an equimolar fall in [Cl~]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135%, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCI infusion, virtually all of the extra Na and Cl~ filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na and Cl~ reabsorption again kept pace with filtration. HCCb" reabsorption also increased, but did not keep pace with filtration; an increased flow of HCC>3~-rich urine resulted, which excreted about 10% of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg" ' at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na and C\" by 50 %, of K by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCI and NaHCCb infusion despite the decreased residence time. However, HCO3~ was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCI as possible from the urine, regardless of the NaCI load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.