Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-1-24
pubmed:abstractText
We investigated the inhibitory effects of ??- or ??-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 ?(½)-AR agonist isoprenaline in rats. We also determined the inhibitory effect of metoclopramide, a dopamine D?-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 ?(½)-AR antagonist propranolol (5 mg/kg, s.c.) and ??-AR antagonist atenolol (2 mg/kg, s.c.) but not by the ??-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 ??-adrenoceptor activity and that salivary amylase activity is useful to detect emetogens with no direct ??-AR activation in rats, a species that does not exhibit vomiting.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-1 Receptor..., http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-2 Receptor..., http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Amylases, http://linkedlifedata.com/resource/pubmed/chemical/Antiemetics, http://linkedlifedata.com/resource/pubmed/chemical/Apomorphine, http://linkedlifedata.com/resource/pubmed/chemical/Atenolol, http://linkedlifedata.com/resource/pubmed/chemical/Butoxamine, http://linkedlifedata.com/resource/pubmed/chemical/Cisplatin, http://linkedlifedata.com/resource/pubmed/chemical/Emetics, http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol, http://linkedlifedata.com/resource/pubmed/chemical/Lithium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Metoclopramide, http://linkedlifedata.com/resource/pubmed/chemical/Propranolol, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-1
pubmed:status
MEDLINE
pubmed:issn
1347-8648
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
69-74
pubmed:meshHeading
pubmed-meshheading:21173550-Adrenergic beta-1 Receptor Antagonists, pubmed-meshheading:21173550-Adrenergic beta-2 Receptor Antagonists, pubmed-meshheading:21173550-Adrenergic beta-Agonists, pubmed-meshheading:21173550-Amylases, pubmed-meshheading:21173550-Animals, pubmed-meshheading:21173550-Antiemetics, pubmed-meshheading:21173550-Apomorphine, pubmed-meshheading:21173550-Atenolol, pubmed-meshheading:21173550-Butoxamine, pubmed-meshheading:21173550-Cisplatin, pubmed-meshheading:21173550-Depression, Chemical, pubmed-meshheading:21173550-Emetics, pubmed-meshheading:21173550-Isoproterenol, pubmed-meshheading:21173550-Lithium Chloride, pubmed-meshheading:21173550-Male, pubmed-meshheading:21173550-Metoclopramide, pubmed-meshheading:21173550-Propranolol, pubmed-meshheading:21173550-Rats, pubmed-meshheading:21173550-Rats, Wistar, pubmed-meshheading:21173550-Receptors, Adrenergic, beta-1, pubmed-meshheading:21173550-Saliva
pubmed:year
2011
pubmed:articleTitle
Possible involvement of ?? receptors in various emetogen-induced increases in salivary amylase activity in rats.
pubmed:affiliation
Development Research Center, Takeda Pharmaceutical Company, Ltd., Osaka, Japan. Fukui_Hideo@takeda.co.jp
pubmed:publicationType
Journal Article