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-agcmist (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 at i 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 a-i-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 α1-adrenoceptor binding sites which might have appeared as a result of the isoproterenol pretreatment of the parotid slices.
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