Abstract
The uptake and efflux of the isotopic tracer 45Ca were compared in dispersed submandibular acini of both control rats and rats treated with seven daily doses of reserpine (0.5 mglkg, i.p.). Tracer uptake occurred in a time-dependent manner in both types of acini and reached 8.4 ± 0.2 and 8.0 ± 0.2 pmol/mg protein, respectively, in acini from control and treated animals after 60 min of incubation. Uptake of tracer was 2.35 nmol/mg DNA in control cells and 4 nmol/mg DNA in cells from treated rats at 60 min. 45Ca uptake (per mg protein) was enhanced in control acini 48% by 20 μmol/L epinephrine: 38% by 50 μmol/L carbachol; and 23% by 10 μmol/L isoproterenol. A similar order of potency was observed when uptake was expressed per mg DNA. In acini from reserpine-treated rats, 45Ca uptake (per mg protein) was increased 53% by epinephrine, 39% by isoproterenol, and only 8% by carbachol. The same enhanced effect of isoproterenol and lack of effect of carbachol were observed when uptake was calculated per mg DNA. In the absence of secretagogue, efflux of 45Ca from tracer-pre-loaded acini was larger in acini from reserpine-treated rats (53%) than in control acini (36%). Whether expressed in terms of mg protein or mg DNA, this efflux was increased in control acini 35% by epinephrine, from 25 to 28% by isoproterenol, and 17% by carbachol. In acini of reserpine-treated rats, epinephrine increased 45Ca efflux 20%, isoproterenol from 25 to 28%, and carbachol from 14 to 15%. The time course of epinephrine- and isoproterenol-induced efflux was also different from that in control cells. Thus, chronic treatment with reserpine altered uptake and efflux of 45Ca in rat submandibular acini. This suggests alterations in secretagogue-sensitive Ca++ pools or gating mechanisms and is likely to underlie disturbances in the Ca++-mediated events of the stimulus-response coupling mechanism, such as fluid, electrolyte, and protein secretion.