Effect of chronic reserpine administration on K+ and amylase release from the rat parotid gland.
After chronic administration of reserpine, slices of the rat parotid gland incubated in vitro were found to release significantly more K+ and significantly less amylase than similar slices from untreated control animals. The extent of K+ release in the gland slices of the drug-treated animals shows no dependency on external Na+ or Ca++ and is probably enhanced because of a decreased activation of K+ uptake by the Na+-K+ pump. This effect may also involve a defective generation of cyclic GMP, which was found to enhance K+ uptake and, thus, to inhibit K+ release in control slices. The inhibition of amylase release observed after treatment with reserpine most likely results from a deficient level or utilization of the energy or nucleotide sources required for enzyme secretion, because a similar inhibition was observed in control slices after incubation in the absence of the purines inosine and adenine. These results indicate that chronic reserpine administration impairs the stimulus-secretion coupling mechanism in the rat parotid gland and results in abnormal responses from both alpha and beta adrenergic receptors.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011941:Receptors, Adrenergic / Q000187:drug effects; D012110:Reserpine / Q000008:administration & dosage / Q000494:pharmacology*; D012964:Sodium / Q000494:pharmacology
D000318:Adrenergic beta-Agonists; D011941:Receptors, Adrenergic; D010042:Ouabain; D012110:Reserpine; D012964:Sodium; D000681:Amylases; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium; D004837:Epinephrine