Effects of Isoproterenol Pretreatment on Phosphatidylinositol Turnover in Rat Parotid Gland

Abstract

The effects of isoproterenol pretreatment on phosphatidylinositol turnover in rat parotid slices were studied to elucidate the relationship between β- and α₁ -adrenoceptors. ³²P-Labeling of phosphatidylinositol in parotid slices was increased by an α₁- and α₂-agonist (epinephrine and norepinephrine) and α₁-agonists (methoxamine and phenylephrine), but not by an α₂-agonist (clonidine) and a β-agonist (isoproterenol). Prazosin inhibited the increase in phosphatidylinositol turnover elicited by epinephrine, but propranolol did not. These results indicate that the stimulation of phosphatidylinositol turnover elicited by adrenergic agonists is mediated by activation of α₁-adrenoceptors in the parotid glands. Isoproterenol pretreatment of the parotid slices caused a significant increase in ³²P-labeling of phosphatidylinositol and a decrease in that of phosphatidic acid. The epinephrine or phenylephrine-induced increase in ³²P-labeling of phosphatidylinositol were further enhanced by the isoproterenol pretreatment of the slices. In the isoproterenol-treated membranes of the parotid glands, [³H]prazosin binding to α₁-receptors increased, but [³H]dihydroalprenolol binding to β-receptors did not. These findings indicate that the acceleration of phosphatidylinositol turnover induced by the isoproterenol pretreatment may be associated with an increase in α-adrenoceptor binding sites which might have appeared as a result of the isoproterenol pretreatment of the parotid slices.