The role of circulating catecholamines in the depletion of parotid acinar granules in conscious rats in the cold.
The possibility that circulating catecholamines might affect parotid gland function during feeding (over a period of 80 min) and cold stress (2-4 degree C) was investigated in rats that had been fasted for 30 h. In the first set of experiments, in which the glands had been sympathectomized by removing both superior cervical ganglia 10-12 days previously, there was a substantial reduction in the density of acinar secretory granules (42% compared with non-fed animals in the cold) and in the total glandular amylase activity (54%). However, similar, or even greater, losses were recorded in rats subjected to additional bilateral adrenal medullectomy and pretreatment with atropine and alpha- and beta-adrenoceptor blockers. The losses were therefore attributed to activation of parasympathetic non-adrenergic, non-cholinergic mechanisms. In a second set of experiments, employing only morphometric assessment, the parasympathetic auriculotemporal nerve was cut on one side in addition to bilateral sympathectomy and, as a further precaution, the animal was atropinized. It was then found that there was a loss of 17% of granules in the parasympathectomized plus sympathectomized gland, but not the contralateral gland, of non-fed cold-exposed rats compared with non-fed animals kept at room temperature. When rats were fed as well as exposed to cold the number of granules in parasympathectomized plus sympathectomized glands fell by 46% compared with similar non-fed animals in the cold and by 55% compared with those at room temperature. After adrenal medullectomy, cold exposure alone had no effect on the granular density of parasympathectomized plus sympathectomized glands but, when combined with feeding, granular loss amounted to 30%. Pretreatment with a combination of alpha- and beta-adrenoceptor blocking agents abolished this effect. Thus circulating catecholamines liberated not only from the adrenal medulla but also from other sources (extraglandular adrenergic nerve terminals and extra-adrenal chromaffin tissue) are able to induce losses in the number of acinar granules in the parasympathectomized plus sympathectomized glands. However, a high degree of sensitization of the parotid acinar cells may be required to allow the response to become manifest.
Asztély
A
A
Department of Pharmacology, Göteborg University, Sweden.
Tobin
G
G
Ekström
J
J
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002395:Catecholamines / Q000097:blood*; D003080:Cold Temperature; D003594:Cytoplasmic Granules / Q000648:ultrastructure*; D005260:Female; D017764:Parasympathectomy; D010306:Parotid Gland / Q000187:drug effects / Q000294:innervation / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017783:Superior Cervical Ganglion; D013562:Sympathectomy
D002395:Catecholamines; D001285:Atropine