The hormonal control of Cl transport was examined in rabbit cortical collecting tubules using the lumen-to-bath 36Cl tracer rate coefficient (K(Cl), nm/s). Tracer movement via Cl-HCO3 exchange was minimized by using HCO3-CO2-free solutions. The electrical driving force was minimized by treating with amiloride. Under these conditions, net Cl transport was zero, yet there was a large K(Cl) that fell 88% on removing bath (trans) Cl. These results are consistent with the mechanism of tracer flux being predominantly Cl self exchange. K(Cl) fell spontaneously with time in vitro; after this decline K(Cl) could be stimulated with 8-bromo-cAMP. cAMP present from the onset of perfusion prevented the time-dependent fall in K(Cl). When tracer movement was restricted to diffusion by eliminating Cl self exchange (0 Cl bath), cAMP had no effect on K(Cl). Although both isoproterenol and vasopressin are known to stimulate adenylate cyclase in this epithelium, only isoproterenol mimicked the cAMP effect on K(Cl). The isoproterenol effect was blocked by either propranolol or prostaglandin E2. Lumen addition of the disulfonic stilbene DIDS had no effect on K(Cl). Lumen addition of furosemide or trichloromethiazide had minimal or no effect. Taken together, these results indicate that Cl self exchange is regulated by β-adrenergic agents acting via cAMP. The lack of an effect of vasopressin suggests cellular heterogeneity in this response to cAMP.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Jan 1 1986|
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