Nephron electrolyte transport and sodium-potassium adenosine triphosphatase activity: influence of nicotine in rat and rabbit.

1. The influence upon mammalian renal epithelial transport of L-nicotine was studied in different types of experiments. 2. The kidney in situ (rat), when infused with nicotine (1 mg hr-1 kg-1 I.V.), lowered its absolute and fractional K+-absorption significantly and reversibly, but Na+-absorption did not change. Effects on glomerular function and an irreversible effect upon epithelial Na+ and K+ absorption were prevailing at higher infused amounts (10 or 50 mg hr-1 kg-1). 3. Single dissected nephron segments (collecting tubule, rabbit) were perfused in vitro, and the Na+ and K+-transtubular net flux was measured while L-nicotine (50 ng/ml.) had been added to the contraluminal side of the epithelium. Both, Na+-absorption and K+-secretion were decreased reversibly. 4. The activity of the Na+-K+-activated ATPase was significantly decreased in the cortical collecting tubule and in the proximal convoluted tubule of the rabbit after incubation of single in vitro dissected nephron segments with L-nicotine (50 or 100 ng/ml.). In contrast, nicotine added to a homogenate of renal cortical tissue had no effect on the Na+-transport enzyme or on key enzymes of glycolysis and gluconeogenesis. 5. These observations on the kidney in situ and on defined, perfused and non-perfused nephrons in vitro suggest that L-nicotine has dose-dependent, direct epithelial and mediated systemic effects on mammalian renal ion transport.