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MAJOR INORGANIC ANIONS present in body fluids, phosphate (HPO& i.e., Pi) and SO4 are handled by the mammalian kidney in a similar manner (14,20a). Both Pi and SO4 are filtered in glomeruli and then reabsorbed, mostly or exclusively in the proximal tubules (14, 20a). The key step in reabsorption of both Pi and SO, from lumen across the proximal tubular epithelium is a co (symport) of the solute coupled with Na+ across the luminal brush-border membrane (BBM), which is energized by a lumen-to-cell directed ([Na+], > [Na+]i) gradient (3, 14, 20a). The Na+-Pi and Na+-SO4 symporters can be distinguished with use of inhibitors; i.e., Na+-Pi symporter is inhibited by arsenate, tungstate (20a), or phosphonoformate (PFA) (17, 18, 21), whereas the Na+-SO4 symporter is specifically blocked by thiosulfate, selenite, and molybdate (2, 20a). Functionally, the Na+-Pi symporter is distinct from Na+-SO4 symporter in terms of its activity, which is highly regulated by multiple short-acting or long-acting hormones (3,9) and by paracrine/autocrine agents such as dopamine (7, 5). In addition, the activity of the THE TWO 0363-6127/93 $2.00 Copyright Na+-Pi symporter is modulated in response to some metabolic alterations such as dietary intake of Pi, fasting, or metabolic acidosis (3,
AJP - Renal Physiology – The American Physiological Society
Published: Aug 1, 1993
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