The processes by which chloride is transported by the cortical and outermedullary collecting tubule have been most extensively studied using in vitro microperfusion of rabbit tubules. Chloride appears to be transported by three major mechanisms. First, Cl can be actively reabsorbed by an electroneutral Cl-HCO3 exchanger localized to the apical membrane of the HCO3-secreting (β-type) intercalated cell. Cl exits this cell via a basolateral Cl channel. This anion exchange process can also operate in a Cl self-exchange mode, is stimulated acutely by β-adrenergic agonists and cAMP, and is regulated chronically by in vivo acid-base status. Second, Cl can diffuse passively down electrochemical gradients via the paracellular pathway. Although this pathway does not appear to be selectively permeabile to Cl, it is large enough to allow for significant passive reabsorption. Third, Cl undergoes recycling across the basolateral membrane of the H+-secreting (α-type) intercalated cell. HCO3 exit from this cell brings Cl into the cell via electroneutral Cl-HCO3 exchange; Cl then exits the cell via a Cl channel. Cl transport is thus required for acidification and alkalinization of the urine. Both of these processes exist in the cortical collecting tubule. Their simultaneous operation allows fine tuning of acid-base excretion. In addition, these transport systems, when functioning at equal rates, effect apparent electrogenic net Cl absorption without changing net HCO3 transport. These systems may play an important role in regulating Cl balance.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Dec 1 1987|
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