The Effects of Methotrexate on Rat Parotid and Submandibular Glands and Their Secretions (Antineoplastic, Protein, Salivary, Amylase Catecholamines)
Mcbride, Robert Kenneth
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https://hdl.handle.net/2142/71441
Description
Title
The Effects of Methotrexate on Rat Parotid and Submandibular Glands and Their Secretions (Antineoplastic, Protein, Salivary, Amylase Catecholamines)
Author(s)
Mcbride, Robert Kenneth
Issue Date
1986
Department of Study
Physiology and Biophysics
Discipline
Physiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Health Sciences, Pharmacology
Abstract
Experimental animals were injected intraperitoneally with methotrexate (15 mg/kg) for 3 days. Parotid and submandibular main ducts were cannulated and saliva flow was evoked by either intravenous infusion of acetylcholine (10 to 100 (mu)g/min) or an intravenous injection of bethanechol (100 (mu)g/kg).
Methotrexate was found to reduce significantly mean food consumption, body weight, and parotid gland wet weights. Experimental animal salivary total gland DNA levels were not different, but total parotid gland RNA, protein, amylase and water content, and submandibular gland RNA were significantly lower compared to controls. Acetylcholine, but not bethanechol, evoked parotid protein and amylase outputs and submandibular protein output from experimental animals were significantly higher than the control groups'. The increased outputs were apparently linked to (beta)-adrenergic receptor activation, since hexamethonium or propranolol eliminated the significant increases while phenoxybenzamine did not. Plasma catecholamine levels were significantly higher in the methotrexate treated animals and probably played a role in the salivary gland (beta)-adrenergic activation. Methotrexate treatment significantly increased the submandibular gland (beta)-adrenergic receptor concentration as determined by ('3)H -dihydroalprenolol receptor binding assays. Muscarinic receptor concentrations determined with ('3)H -quinuclidinyl benzilate were not changed.
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