Abstract

Acinar cells of the rat parotid gland are in intimate contact with adrenergic nerves, arousing from the ganglion cervicale superior (Bloom et al. 1977). The sympathetic nerves or circulating catecholamines exert their effects by activating α‐adrenoceptors (electrolyte and water secretion) or β‐adrenoceptors (enzyme secretion) (Batzri et al. 1971, Carlsöö et al. 1981). It is now well established that the β‐adrenoceptors can be divided in two subclasses, β1 and β2, present in different proportions depending on the tissue examined (Lands et al. 1967, Carlsson et al. 1972, Barnett et al. 1978, Minneman et al. 1979a). The concentrations of the two subtypes are regulated independently (Minneman et al. 1979b) and their molecular structure seems to be different (Venter et al. 1981). The β1, ‐subtype is dominating in normal rat parotid glands (Carlsöö et al. 1981, Ludford & Talamo 1980). Supersensitivity occuring in salivary glands after interruption of the sympathetic nerve supply in adult animals is usually associated with an increased number of the β‐adrenoceptors (Ludford & Talamo 1980, Stefano & Perec 1981). In the present work we have studied the effect of neonatal sympathetic denervation of the rat parotid gland on the binding of the β‐adrenoceptor radioligand 3H‐dihydroalprenolol (3H‐DHA) and on the β‐adrenoceptor‐induced amylase secretion. The results suggest that the normal dominance of the β1‐adrenoceptors is lost after neonatal sympathetic denervation. Hence, an intact sympathetic nervous system may be of major importance during the development of the β‐adrenoceptor population.

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