The kidneys combine two qualities that almost seem paradoxical: a stabilizing function to serve solute and fluid homeostasis and a dynamic response to perturbations of the internal environment, particularly sodium loading. The paper by Thomson (6) in this issue seeks to explain how one of the key stabilizing mechanisms in the kidneys, the tubu-loglomerular feedback mechanism (TGF), is overruled by (macula densa) nitric oxide release after induction of experimental renal failure to allow facilitation of sodium excretion to maintain sodium balance.
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