title: Reflex-elicited increases in female rat parotid protein synthesis involving parasympathetic non-adrenergic, non-cholinergic mechanisms.
abstract: Normal rats or rats parasympathetically denervated on one side by cutting the auriculo-temporal nerve were maintained on a liquid diet for 1 week. After fasting overnight, experimental rats were then offered hard, pelleted food over a period of 2 h, while unfed animals served as controls. The reflex-induced increase in the [3H]leucine incorporation into trichloroacetic acid-insoluble material of the parotid glands following intake of the food in the presence of the muscarinic blocker atropine and alpha- and beta-adrenoceptor antagonists was greater (104%) than in the absence of the blockers (75%) in normal rats. The picture was the same when the innervated glands of rats subjected to unilateral parasympathetic denervation were examined. In this case, the protein synthesis increased by 108% in the presence of the blockers and by 63% in their absence. Analysis of the parasympathetically denervated and contralateral innervated glands revealed no support for a cholinergic or adrenergic contribution to this response. The increase in protein synthesis in the innervated glands was 86% in the rats treated with atropine, whilst it was 76% in those treated with alpha- and beta-adrenoceptor antagonists. The protein synthesis in the denervated glands increased by 57% in the absence of receptor blockade. Neither atropine (51%), nor a- and b-adrenoceptor antagonists (52%), nor a combination of the three blockers (55%) affected the response of the denervated glands. A large part of the response in the presence of the traditional autonomic receptor blockers was thus dependent on the parasympathetic auriculo-temporal nerve. Under natural feeding conditions, the parasympathetic non-adrenergic, non-cholinergic (NANC) mechanisms are likely to contribute to the synthesis of secretory proteins.
authors.affiliation: Department of Pharmacology, Institute of Physiology and Pharmacology, Göteborg, University, Box 431, SE-405 30 Göteborg, Sweden. jorgen.ekstrom@pharm.gu.se
authors.forename: J
authors.initials: J
authors.lastname: Ekström
authors.forename: A C
authors.initials: AC
authors.lastname: Reinhold
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001835:Body Weight; D004032:Diet; D005260:Female; D007930:Leucine / Q000737:chemistry / Q000378:metabolism; D009929:Organ Size; D017764:Parasympathectomy; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010276:Parasympatholytics / Q000494:pharmacology; D010306:Parotid Gland / Q000294:innervation* / Q000378:metabolism*; D014176:Protein Biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000502:physiology*; D014316:Tritium / Q000737:chemistry / Q000378:metabolism
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics; D014316:Tritium; D001285:Atropine; D007930:Leucine