Effect of Chronic Reserpine Administration on K+ and Amylase Release from the Rat Parotid Gland

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Abstract

Summary

The release of K+ and of amylase were compared in parotid gland slices from control and reserpine-treated rats during incubation in an enriched, oxygenated medium. After 10 min of incubation in the presence of 2 × 10--5 M epinephrine, net K+ release was 17% in control slices and 32% in those from the treated animals. When 1 mM ouabain was added to the incubation medium in the presence of the hormone, K+ release was similar in the two types of slices and reached 50%. Omission of Ca++ from the incubation medium reduced the epinephrine-induced net release in control slices to 9%, but not in those of reserpine-treated rats, which still showed a 28% release. The divalent cation ionophore A 23187 also induced a significantly greater K+ release in the slices of the treated animals. In the absence of ouabain, the 8-bromo derivative of cyclic GMP inhibited basal K+ release in control slices and caused a small, but significant K+ uptake in the slices of the treated animals. Amylase release after 30 min of incubation in the presence of either 2 × 10--5 M epinephrine or 10--5 M isoproterenol was 50% in control slices and 17% in slices from reserpine-treated rats. Amylase release was also reduced in the slices of the treated animals in the presence of the dibutyryl derivative of cyclic AMP. Release of this enzyme was not affected by the presence of ouabain or by the omission of Ca++ from the incubation medium, but was significantly reduced in the slices of both control and reserpine-treated rats when the Na+ concentration of the incubation medium was reduced to 21 mM. Amylase release was reduced in control slices to the levels observed in slices of reserpine-treated rats when the purines inosine and adenine were omitted from this medium. The chronic administration of reserpine, thus, results in a significantly increased release of K+ and in a significantly decreased release of amylase from rat parotid gland slices. These results demonstrate that chronic reserpine administration inpairs the in vitro responses of both a and β adrenergic receptors in the rat parotid gland.

Prolonged reserpine administration impairs the stimulus-secretion coupling mechanism in the parotid glands, leading to an altered secretion of ions and of macromolecules. Because the reserpine-treated rat has been proposed as an animal model for cystic fibrosis, these findings suggest that the secretory abnormality observed in this disease is also related to an abnormal stimulus-secretion coupling mechanism during the secretory response to physiologic stimulants.

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