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Journal of Experimental Biology, Vol 189, Issue 1 13-36, Copyright © 1994 by Company of Biologists

JOURNAL ARTICLES

UREA PRODUCTION, ACID-BASE REGULATION AND THEIR INTERACTIONS IN THE LAKE MAGADI TILAPIA, A UNIQUE TELEOST ADAPTED TO A HIGHLY ALKALINE ENVIRONMENT

C Wood, H Bergman, P Laurent, J Maina, A Narahara and P Walsh

The Lake Magadi tilapia, Oreochromis alcalicus grahami, thrives in highly alkaline geothermal springs and pools surrounding Lake Magadi, Kenya (control pH=9.9, CCO2=173 mmol l-1), has a functional hepatic ornithine­urea cycle (OUC) and excretes all nitrogenous waste as urea-N at variable rates (JUrea) related to O2 consumption (M·O2). The mean value of JUrea/M·O2 (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 [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 CCO2 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 CCO2 of 0 mmol l-1 resulted in intermediate levels of N/O2 and internal acid­base 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 acid­base regulation.
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© The Company of Biologists Ltd 1994