Urea production, acid–base regulation and their interactions in the lake magadi tilapia, a unique teleost adapted to a highly alkaline environment
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ABSTRACTThe Lake Magadi tilapia, Oreochromis alcalicus grahami, thrives in highly alkaline geothermal springs and pools surrounding Lake Magadi, Kenya (control ), has a functional hepatic ornithine–urea cycle (OUC) and excretes all nitrogenous waste as urea-N at variable rates (JUrea) related to O2 consumption . The mean value of was high for fish but below the theoretical maximum (approximately 0.27) for 100 % aerobic respiration of protein, so an exogenous source of substrates is not required to explain the observed JUrea. JUrea was insensitive to thiourea. Urea excretion occurred largely (80 %) through the gills, but urea-N was also present in bile and urine. Control blood pHe, pHi and [HCO3−] (approximately 8.1, 7.6 and 15 mmol l−1, respectively, at approximately 32 °C) were extremely high. When fish were exposed to lake water titrated with HCl and aerated to remove CO2, N/O2 progressively declined. At a lake water pH of 7.05 and of 0 mmol l−1, N/O2 was reduced by 80 % and an intense metabolic acidosis occurred (pHe=7.04, [HCO3−]=1.5 mmol l−1). Restoration of control water pH 9.9 at a of 0 mmol l−1 resulted in intermediate levels of N/O2 and internal acid–base status. Additional experiments confirmed that urea production was inhibited by low pHe, was dependent on blood [HCO3−] with a Km of 3.06 mmol l−1 and was insensitive to acetazolamide. While metabolic acidosis clearly inhibited OUC ureagenesis, the system appeared to be saturated with HCO3− under control conditions so that additional basic equivalent loading would not stimulate ureagenesis. Urea production in the Lake Magadi tilapia does not appear to remove exogenous HCO3− or to play a role in normal acid–base regulation.
