Plasma membrane desialylation and DNA synthesis are induced via adrenergic receptors of the beta 1-subtype in mouse parotid glands.

Induction of DNA synthesis and plasma membrane desialylation in the early prereplicative period in isoproterenol-stimulated mouse parotid glands seem to occur in a close relationship. beta 1, beta 2 or both subtypes of adrenergic receptors could be involved in those responses. To discriminate between those alternatives, dose-dependency studies were addressed to assess the abilities of the selective beta-adrenergic agonists dobutamine (beta 1) and salbutamol (beta 2) to induce plasma membrane desialylation and DNA synthesis. Likewise, the abilities of the selective beta-adrenoceptor antagonists atenolol (beta 1) and ICI 118,551 (beta 2) to interfere with the induction of both responses were also studied. Dobutamine was found to be at least 10-fold more potent than salbutamol in inducing DNA synthesis whereas ICI 118,551 was much weaker than atenolol, as inhibitor of the agonist-induced DNA synthesis. On the other hand, dobutamine was also more potent than salbutamol in provoking plasma membrane desialylation. However, whenever an increase in the rate of DNA synthesis was induced by either agonist, a constant 50% reduction in the levels of sialic acid in the plasma membranes was observed. In the same direction, atenolol, at variance to ICI 118,551, was able to produce a full suppression of the plasma membrane desialylation induced by either selective agonist. Taken together, these results suggest that in mouse parotid glands, both DNA synthesis and plasma membrane desialylation during the early prereplicative period are induced preferentially via adrenergic receptors of the beta 1-subtype.