| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2023251 | Regulatory Peptides | 2008 | 7 Pages |
Recent studies show I.V. administered pentagastrin and cholecystokinin to evoke protein/amylase secretion from the rat parotid gland and to stimulate gland protein synthesis, the two phenomena being abolished by cholecystokinin receptor antagonists. In the rat parotid gland, non-adrenergic, non-cholinergic transmission mechanisms contribute to secretion of fluid and protein/amylase. Since cholecystokinin may act as a neurotransmitter, activation of cholecystokinin receptors of the gland might contribute to the parasympathetic nerve-evoked secretion. In this study, the parasympathetic innervation was stimulated in non-atropinized (in periods of 2 min) or atropinized (in periods of 3 min) pentobarbitone-anaesthetized rats before and after administration of the cholecystokinin-A receptor antagonist lorglumide (48 mg/kg, I.V.) and the cholecystokinin-B receptor antagonist itriglumide (5.5 mg/kg, I.V.). The non-adrenergic, non-cholinergic transmission fatigues rapidly resulting in declining responses. Therefore, atropinized rats, not receiving the cholecystokinin receptor antagonists, had to serve as controls. Neither at a stimulation frequency of 10 Hz nor of 40 Hz were the secretory responses of the atropinized rats affected by the receptor antagonists. After lorglumide, the saliva volume and the amylase output were (expressed as percentage of the response to the stimulation period before the administration of the antagonist) 98.0 ± 3.8% (vs. control 91.1 ± 4.0%) and 91.9 ± 4.9% (vs. 87.7 ± 3.7%) at 10 Hz, respectively, and 79.8 ± 4.5% (vs. 77.3 ± 2.1%) and 73.6 ± 5.3% (vs. 71.7 ± 2.3%) at 40 Hz, respectively. After itriglumide, the corresponding percentage figures for saliva volume and amylase output were, at 10 Hz, 99.5 ± 8.9% (vs. 92.0 ± 2.8%) and 95.8 ± 11.8% (vs. 89.2 ± 6.4%), respectively, and, at 40 Hz, 74.0 ± 3.1% (vs. 79.6 ± 2.2%) and 66.6 ± 3.3% (vs. 63.9 ± 6.0%), respectively. Similarly, the antagonists were without effect on the parotid secretory responses of non-atropinized rats subjected to stimulation at 10 Hz. Thus, under physiological conditions, the cholecystokinin receptors of the parotid gland are likely to be stimulated by circulating hormones rather than by nervous activity.
