Renal homeostasis and tubuloglomerular feedback.

PURPOSE OF REVIEW: We review some basic homeostatic principles that are frequently disregarded to provide boundary conditions to test any new theory containing new details. Homeostasis as applied to total body salt is discussed with a linear model for salt homeostasis that is extraordinarily simple wherein total body salt drives the salt excretion. The basics of tubuloglomerular feedback (TGF) and its implications for salt homeostasis are then reviewed. RECENT
FINDINGS: Advances in the field discussed include new details on the apical and basolateral transport of sodium chloride (NaCl) in the macula densa cells during TGF response, direct evidence of contribution of TGF to renal autoregulation and the description of vasodilatory adenosine A2b receptors in the 'efferent' TGF response. Finally, recent information about the role of proximal tubular microvilli as mechanosensors in the flow-dependent tubular reabsorption as a mechanism to explain glomerulotubular balance is reviewed.
SUMMARY: Notwithstanding the complexity of salt balance at a molecular level, the overall salt homeostasis is simple. Various natritropic nerves and hormones stabilize any disturbance in salt balance. A change in glomerular filtration rate (GFR) brought about by these natritropes will be partially counteracted by the impact of TGF on nephron function. Thus, by stabilizing GFR, TGF reduces the usefulness of GFR as an instrument of salt balance, and lessens the efficiency of salt homeostasis.