Urea Production, Acid-base Regulation And Their Interactions In The Lake Magadi Tilapia, A Unique Teleost Adapted To A Highly Alkaline Environment

Abstract

The Lake Magadi tilapia, Oreochromis alcalicus grahami, thrives in highly alkaline geothermal springs and pools surrounding Lake Magadi, Kenya (control pH=9.9, CCO·=173mmoll21), has a functional hepatic ornithine–urea cycle (OUC) and excretes all nitrogenous waste as urea-N at variable rates (JUrea) related to O2 consumption (M · O·). The mean value of JUrea/M · O· (N/O2=0.183) 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 [HCO32] (approximately 8.1, 7.6 and 15mmoll21, 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 CCO· of 0mmoll21, N/O2 was reduced by 80 % and an intense metabolic acidosis occurred (pHe=7.04, [HCO32]=1.5mmoll21). Restoration of control water pH 9.9 at a CCO· of 0mmoll21 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 [HCO32] with a Km of 3.06mmoll21 and was insensitive to acetazolamide. While metabolic acidosis clearly inhibited OUC ureagenesis, the system appeared to be saturated with HCO32 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 HCO32 or to play a role in normal acid–base regulation.