Chloride transport in the rat S1 proximal tubule
Wong, K.R.; Berry, C.A.; Cogan, M.G.
American Journal of Physiology 268(4 Pt 2): F723-F729
1995
ISSN/ISBN: 0002-9513 PMID: 7733330 Document Number: 448808
In vivo microperfusion was used to elucidate the modes and regulation of the powerful chloride transport system resident in the rat early (S1) proximal convoluted tubule (PCT). From a complete, glomerular ultrafiltrate-like perfusate, omission of organic solutes reduced chloride absorption by 93 peq cntdot mm-1 cntdot min-1 (302 +- 10 to 209 +- 24, P lt 0.001). From a high-chloride perfusate (a relatively pure NaCl solution devoid of bicarbonate and organic solutes), luminal addition of the active transport inhibitor cyanide reduced chloride absorption by 153 peq cntdot mm-1 cntdot min-1 (632 +- 17 to 479 +- 9, P lt 0.001). Active transport was also estimated directly as 121 +- 4 peq cntdot mm-1 cntdot min-1 using a solution in which sodium isethionate isosmotically replaced bicarbonate and organic solutes, preventing development of a chloride gradient. Intravenous angiotensin II caused a stimulation of chloride absorption from a high-chloride perfusate by 55 peq cntdot mm-1 cntdot min-1 (632 +- 17 to 687 +- 14,P lt 0.05), which was partially cyanide-sensitive (510 +- 6 peq cntdot mm-1 cntdot min-1). In conclusion, the components of the normal SI PCT chloride reabsorption ( apprx 300 peq cntdot mm-1 cntdot min-1) from the glomerular ultrafiltrate consist of the following: active transport (4050%), which can be regulated by angiotensin II; sodium-coupled organic solute transport (30%); and passive, chloride concentration gradient-driven transport (20-25%).