Regulation of Salivary Kallikrein Secretion in the Rat Submandibular Gland
- 1 May 1977
- journal article
- research article
- Published by Wiley in Acta Physiologica Scandinavica
- Vol. 100 (1) , 33-44
- https://doi.org/10.1111/j.1748-1716.1977.tb05919.x
Abstract
Unstimulated pairs of rat submandibular glands were compared with regard to their wet weight, total protein content and kallikrein [E.C. 3.4.4.21] activity quantitated by Bz-Agr-OEt[benzyl-argino-O-ethoxy]-esterase and kallikrein antigenic activity. Paired glands from the same animal were comparable, whereas differences from one animal to another were considerable. One of 2 paired glands was extirpated and used as control, and the other was subsequently subjected to stimulation. Salivary secretion was induced parasympathomimetically (i.v. injections of pilocarpine; perfusion with acetylcholine and electrical stimulation of the ductal nerve plexus near the gland hilus) or sympathomimetically (cervical sympathetic nerve stimulation with or without administration of .alpha.- or .beta.-adrenergic blocker; perfusion with epinephrine, norepinephrine or isoproterenol). The effect was studied by measuring the change in total gland kallikrein content and by quantitation of kallikrein in saliva. A small secretion of kallikrein was always observed. However, .alpha.-adrenergic stimulation was 40 and 1500-fold more effective in releasing kallikrein than .beta.-adrenergic and parasympathomimetic stimulation, respectively. Also, significantly more kallikrein was released by .beta.-adrenergic than parasympathomimetic stimulation. Immunohistochemistry confirmed the observed depletion of kallikrein following .alpha.-adrenergic stimulation. No alteration in kallikrein localization was observed in stimulated glands.This publication has 15 references indexed in Scilit:
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