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Abnormal 45Ca Fluxes in Dispersed Submandibular Acini of Rats Treated with Reserpine

Wenner-Gren Institute, University of Stockholm, Sweden

J.R. Martinez

Department of Child Health, University of Mis,souri Sohool of Medicine. Columbia, Missouri 65212

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.

Journal of Dental Research, Vol. 66, No. 8, 1294-1299 (1987)
DOI: 10.1177/00220345870660080101


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