Open AccessEffects of Isoproterenol Pretreatment on Phosphatidylinositol Turnover in Rat Parotid Gland
Author(s) -
Atsushi Miyamoto,
Toyoaki Akino,
Hideyo Ohshika
Publication year - 1986
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.42.63
Subject(s) - phosphatidylinositol , endocrinology , prazosin , phenylephrine , medicine , chemistry , agonist , adrenergic receptor , stimulation , alpha (finance) , parotid gland , epinephrine , isoprenaline , propranolol , receptor , biology , antagonist , biochemistry , signal transduction , dentistry , blood pressure , construct validity , nursing , patient satisfaction
The effects of isoproterenol pretreatment on phosphatidylinositol turnover in rat parotid slices were studied to elucidate the relationship between beta- and alpha 1-adrenoceptors. 32P-Labeling of phosphatidylinositol in parotid slices was increased by an alpha 1- and alpha 2-agonist (epinephrine and norepinephrine) and alpha 1-agonists (methoxamine and phenylephrine), but not by an alpha 2-agonist (clonidine) and a beta-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 alpha 1-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 alpha 1-receptors increased, but [3H]dihydroalprenolol binding to beta-receptors did not. These findings indicate that the acceleration of phosphatidylinositol turnover induced by the isoproterenol pretreatment may be associated with an increase in alpha 1-adrenoceptor binding sites which might have appeared as a result of the isoproterenol pretreatment of the parotid slices.