Acini isolated from the rat submandibular gland showed uptake of³⁶Cl in the absence of added test substances. A steady state of³⁶Cl content corresponding to 9.5±0.7 nM/mg protein was attained in 4–5 min and maintained for 25–30 min. This uptake of³⁶Cl was reduced 40–50% by previous exposure to 10⁻³ M furosemide, 10⁻³ M ouabain, or K⁺-free medium. The steady state of³⁶Cl content was reduced 34% by 10⁻⁶ M acetylcholine while exposure of the acini to the stilbene sulfonic DIDS (10⁻³ M) did not modify³⁶Cl uptake either in the absence (basal) or presence of acetylcholine. Acetylcholine caused a rapid reduction of³⁶Cl from tracer-preloaded acini (42% in 1 min), while furosemide induced a slower reduction of tracer content (45% in 9 min). Acetylcholine increased the rate of reduction of tracer content induced by furosemide and the latter caused a further reduction in³⁶Cl content of acini previously exposed to acetylcholine. It is concluded that a furosemide-sensitive Cl uptake is present in rat submandibular acini, which depends on the Na⁺ gradient generated by the Na, K pump and on external K⁺. These findings suggest that a Na−K−Cl cotransport system driven by the Na, K pump is present in salivary acinar cells. Acetylcholine induces a rapid net efflux of³⁶Cl, which probably masks any effect that this secretagogue may have on Cl uptake. The lack of effect of DIDS on³⁶Cl uptake suggests that anion exchange transport systems are either not present in rat submandibular acini or can only be ascertained under different incubation conditions.

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