title: Possible involvement of β₁ receptors in various emetogen-induced increases in salivary amylase activity in rats.
abstract: We investigated the inhibitory effects of β₁- or β₂-adrenoceptor (AR) antagonists on salivary amylase secretion produced by various emetic agents, such as cisplatin, apomorphine, and lithium chloride (LiCl), or the non-emetic agent β(½)-AR agonist isoprenaline in rats. We also determined the inhibitory effect of metoclopramide, a dopamine D₂-receptor antagonist, on increases in the salivary amylase activity induced by apomorphine or granisetron, a 5-HT(3)-receptor antagonist, on LiCl-induced increased salivary amylase activity. Isoprenaline (0.01 mg/kg, s.c.) produced an increase in salivary amylase and the increase was inhibited by the β(½)-AR antagonist propranolol (5 mg/kg, s.c.) and β₁-AR antagonist atenolol (2 mg/kg, s.c.) but not by the β₂-AR antagonist butoxamine (8 mg/kg, s.c.). The increased amylase activity induced by cisplatin (15 mg/kg, i.v.), apomorphine (3 mg/kg, s.c.), or LiCl (120 mg/kg, i.p.) was inhibited significantly by atenolol (2 mg/kg, s.c.) but not by butoxamine (8 mg/kg, s.c.). In addition, increases in amylase activities induced by apomorphine and LiCl were inhibited significantly by metoclopramide (10 mg/kg, i.v.) and granisetron (3 mg/kg, i.v.), respectively. These results suggest that salivary amylase secretion induced by various emetogens is involved in β₁-adrenoceptor activity and that salivary amylase activity is useful to detect emetogens with no direct β₁-AR activation in rats, a species that does not exhibit vomiting.
authors.affiliation: Development Research Center, Takeda Pharmaceutical Company, Ltd., Osaka, Japan. Fukui_Hideo@takeda.co.jp
authors.forename: Hideo
authors.initials: H
authors.lastname: Fukui
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Suyama
authors.forename: Takako
authors.initials: T
authors.lastname: Iwachido
authors.forename: Eri
authors.initials: E
authors.lastname: Miwa
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology; D058672:Adrenergic beta-2 Receptor Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000009:adverse effects; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D000932:Antiemetics / Q000494:pharmacology; D001058:Apomorphine / Q000009:adverse effects; D001262:Atenolol / Q000494:pharmacology; D002078:Butoxamine / Q000494:pharmacology; D002945:Cisplatin / Q000009:adverse effects; D003864:Depression, Chemical; D004639:Emetics / Q000009:adverse effects*; D007545:Isoproterenol / Q000009:adverse effects; D018021:Lithium Chloride / Q000009:adverse effects; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018342:Receptors, Adrenergic, beta-1 / Q000502:physiology*; D012463:Saliva / Q000201:enzymology*
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D000318:Adrenergic beta-Agonists; D000932:Antiemetics; D004639:Emetics; D018342:Receptors, Adrenergic, beta-1; D002078:Butoxamine; D001262:Atenolol; D011433:Propranolol; D000681:Amylases; D018021:Lithium Chloride; D008787:Metoclopramide; D007545:Isoproterenol; D001058:Apomorphine; D002945:Cisplatin