Calcium and norepinephrine levels of rat salivary glands after terbutaline, dobutamine or isoproterenol.

Present data show that a dose-related increase in calcium concentration [Ca] of submandibular glands of rat occurred after 6 days of twice daily administration of 25, 50 or 75 mg/kg b. wt. doses of the beta 1-adrenergic agonist, dobutamine, or the beta 2-adrenergic agonist, terbutaline. The beta 1-adrenergic receptor was responsible for mediation of these changes with both agonists since the effects of either agonist were prevented when a 10 mg/kg dose of the beta 1-antagonist, atenolol, was injected 20 min prior to the agonist, and the increase induced by either agonist was not prevented when the beta 1-adrenergic antagonist, butoxamine, was given prior to each agonist. Dobutamine caused more marked increases in [Ca] than did terbutaline. The parotid gland, however, showed a decrease with both agonists, and that caused by dobutamine was greater than that caused by terbutaline. Neither antagonist had any effect on the agonist-induced changes in the parotid gland. Reasons for the differences in response of the two glands are suggested. It does not appear, however, that, as suggested previously, the increase in the [Ca] of the submandibular gland is dependent on depletion of glandular levels of norepinephrine (NE). Of the agonists, only dobutamine caused a decrease in glandular concentration of NE, as well as total NE of the gland. With isoproterenol (ISO), NE concentration of parotid and submandibular was reduced, but with terbutaline only that of parotid was reduced. changes in total glandular NE were not found in either gland with either ISO or terbutaline. Thus, the decrease in concentration was a consequence of the increased mass of gland. With cyclocytidine (CC), both NE concentration and total NE were reduced, even though gland size increased. With reserpine (RES), NE concentration as well as total NE were markedly reduced (87-90%), and no change in gland size occurred. It is suggested, on the basis of present data, that prolonged activation of beta 1-adrenoceptors is the cause of the calcium accumulation, and that reduction in NE is not the cause of the calcium increase, but may only be a coincident event. Even with sympathectomy (here induced by reserpine), activation of beta-receptors over a long period of time is suggested as the cause of the calcium change, not the depletion of NE. The present data also provide the first evidence that CC causes NE depletion.