Abstract
A model of steady-state hypocitricemia, characterized by hypocitraturia and reduced kidney cortex citrate, has been demonstrated in the rate chronically exposed to environmental heat. The renal citrate extraction ratio remains unchanged. The physiological mechanism that brings about the reduction in circulating citrate has not been determined. Hypocitraturia likely results from a decreased filtered citrate load. Although it is generally contended that filtered citrate load. Although it is generally contended that alkalosis increases and acidosis decreases renal excretion of citrate, observations of mild alkalosis and hypocitraturia during heat exposure suggest that factors other than pH can alter renal handling of citrate. Kidney mitochondrial function, as determined by in vitro measurements of citrate-stimulated respiratory rates and specific activities of isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and cytochrome c oxidase, appears to be unaffected by environmental heat.
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