Parasympathetic non-adrenergic, non-cholinergic reflex secretion of parotid acinar granules in rats pretreated with atropine and adrenoceptor antagonists

Asztély, A.; Tobin, Gunnar; Ekström, Jørgen

doi:10.1016/0167-0115(94)90071-x

Cited by 19 publications

(17 citation statements)

References 13 publications

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“…Each animal was treated as described, and at the designated times, submandibular and parotid glands were perfusion fixed as described below. The drug dosages and exposure times were chosen according to comparable previous studies (2,(21)(22)(23).…”

Section: Methodsmentioning

confidence: 99%

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Gresz

Kwon

Gong

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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In vitro studies of cultured salivary gland cells and gland slices have indicated that there may be regulated translocation of aquaporin (AQP)-5 between the apical plasma membrane and intracellular compartments of the secretory cells. However, it remains unknown whether AQP-5 in salivary glands is subject to regulated trafficking in vivo. To examine this possibility, we have investigated the subcellular localization of AQP-5 in rat parotid and submandibular glands fixed in vivo under conditions of stimulated or inhibited salivary secretion. Immunofluorescence and immunoelectron microscopy was used to determine the subcellular distribution of AQP-5 in control conditions following the stimulation of secretion with pilocarpine (a muscarinic agonist) or epinephrine (an α-adrenoceptor agonist) or during inhibition of basal secretion with atropine (a muscarinic antagonist) or phentolamine (an α-adrenoceptor antagonist). Under control conditions, >90% of AQP-5 was associated with the apical plasma membrane of acinar and intercalated duct cells, with only rare gold particles associated with intracellular membrane domains. Pilocarpine treatment dramatically increased saliva production but had no discernible effect on AQP-5 distribution. However, the increased salivary secretion was associated with luminal dilation and the appearance of a markedly punctate AQP-5 labeling pattern due to clustering of AQP-5 at the microvilli (especially evident in the parotid gland) after 10 min of drug injection. No changes in the subcellular localization of AQP-5 were seen in response to epinephrine, atropine, or phentolamine treatment compared with control tissues. Thus AQP-5 is localized predominantly in the apical plasma membrane under control conditions, and neither the onset nor the cessation of secretion is associated in vivo with any significant short-term translocation of AQP-5 between intracellular structures and the apical plasma membrane.

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Section: Methodsmentioning

confidence: 99%

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Gresz

Kwon

Gong

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…These differences could reflect adaptation to the loss of the sympathetic innervation. The increased sensitivity of the secretory cells following sympathectomy (Ekstrom & Wahlestedt, 1982;Ekstrom, Mansson & Tobin, 1983) is probably the main cause of the larger NANC-induced secretory responses of sympathetically denervated glands to food intake previously recorded (Ekstrom et al 1993;Asztely et al 1994a), the decrease in the number of acinar granules and glandular amylase activity being, respectively, 50 versus 30% in intact glands. It is possible, however, that the larger percentage reductions in the contents of VIP and NPY in sympathetically denervated glands compared with those in the intact glands also contributed to the difference in magnitude of the effector responses.…”

Section: Discussionmentioning

confidence: 99%

“…These doses have previously been shown to achieve an effective blockade of the respective receptors (Ekstrom et al 1993;Asztely et al 1994a). Food and water were offered ad libitum for 80 min (between 9 and 11 p.m.).…”

Section: Feedingmentioning

confidence: 99%

Depletion of vasoactive intestinal peptide and substance P in parotid glands of atropinized rats during reflex secretion

Asztély¹,

Ekman²,

Tobin³

et al. 1996

Experimental Physiology

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SUMMARYRats previously starved for 30 h were offered hard chow over a period of 80 min, and the effect of eating on the parotid gland content of vasoactive intestinal peptide (VIP), substance P and neuropeptide Y (NPY) was examined. In rats pretreated with I.P. atropine and o-and ,b-adrenoceptor blocking agents, the total amounts of VIP and substance P were reduced after feeding by 23 and 42 %, respectively; in contrast the NPY content was not significantly affected. Similarly, in animals given atropine alone the VIP content was reduced by 25 % and substance P by 40 % after feeding. In the absence of autonomic receptor blockade, there was no loss of parotid neuropeptide content in response to feeding. Neither an intact sympathetic innervation nor a capsaicin-sensitive sensory innervation was a prerequisite for depletion of parotid neuropeptides in the presence of atropine and adrenoceptor blockers. The observed decrease in neuropeptide content is thought to reflect an imbalance between peptide release from nerve terminals and their replenishment by axonal transport, this imbalance resulting from the unusually high demands on the parasympathetic non-adrenergic, non-cholinergic (NANC) mechanism. Under normal conditions salivary peptidergic mechanisms are spared as seen in the absence of autonomic receptor blockade.

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“…VIP and substance P caused parotid acinar degranulation, the losses in granular number being 29 %I and 18 %, respectively. These findings make VIP and substance P likely contributors to the non-adrenergic, non-cholinergic-indud degranulation that occurs in response to electrical stimulation of the parasympathetic innervation at 40 Hz or to mastication or taste (Ekstrom et al 1988(Ekstrom et al , 1996Asztely et al 1994;Ekstrom, 2001). There was, however, no loss in acinar granule number in response to neurokinin A.…”

Section: Discussionmentioning

confidence: 99%

“…Further, the major part of the acinar degranulation occurring in response to mastication or taste stiinulus may be attributed to the non-adrenergic, non-cholinergic mechanisms operating in the parasympathetic nerve (Asztely et al 1994;Ekstrom, 2001). …”

Section: Discussionmentioning

confidence: 99%

Acinar degranulation in the rat parotid gland induced by neuropeptides

Ekström

2001

Experimental Physiology

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Vasoactive intestinal peptide (VIP, 4 pg kg-' min-'), substance P (3 pg kg-' min-') and neurokinin A (2.5 pg kg-' min-') were infused intravenously for 30 min in anaesthetized rats and the effects of these peptides on the parotid gland were examined. VIP reduced the numerical density of parotid acinar secretory granules, storing proteins, by 29 ' ' A and the glandular amylase activity by 33 %. Substance P reduced the number of secretory granules by 18 o/u but the amylase activity was unchanged. These results make VIP and substance P likely contributors to the parasympathetic non-adrenergic, non-cholinergic (NANC)-evoked parotid acinar degranulation. Neurokinin A, on the other hand, caused no reduction in granular number but reduced the glandular amylase activity by 19%, indicating vesicular protein secretion. Experimental Physiology (2001) 86.6, 733-738.The parotid gland of the rat has served as model organ for studies on parasympathetic non-adrenergic, non-cholinergk (NANC) secretory mechanisms (Ekstrom, 1999). The gland looses its content of acinar secretory granules, storing secretory proteins, upon electrical stimulation of the parasympathetic innervation in the anaesthetized rat in the presence of atropine and a-and /I-adrenoceptor antagonists (Ekstrom et al. 1988(Ekstrom et al. , 1996. There is also a parasympathetic nerve-evoked acinar degranulation, in the presence of the autonomic receptor blockers, in the conscious animal in response to mastication during feeding (Ekstrom et al. 1993) and to ascorbic acid applied on the tongue (Ekstrom, 2001). Parasympathetic nerve activity, electrically or reflexly elicited, releases the neuropeptides substance P and vasoactive intestinal peptide (VIP) from the parasympathetic nerve fibres of the gland (Ekstrom et al. 1985; AsztCly et al. 1996). Upon intravenous administration substance P causes the gland to secrete a copious flow of saliva poor in protein, while VIP evokes a small, viscous and very protein-rich flow of saliva (Ekstrom et al. 1983). Neurokinin A, like substance P a member of the tachykinin family, also causes secretion of parotid saliva but is less potent than substance P. Furthermore, the amylase concentration is higher in the neurokinin A-induced saliva than in the substance P-induced saliva, suggesting that the two tachykinins may act on different populations of tachykinin receptors in the gland. These tackykinins and VIP are confined to periacinar parasympathetic nerve fibres (Ekstrom, 1999).Substance P, neurokinin A and VIP are possible transmitters involved in the parasympathetic non-adrenergic, noncholinergic-induced exocytotic response of the parotid gland. Therefore, it was investigated whether administration of these three neuropeptides causes granular depletion of the parotid acinar cells. Observations were also made on the effect on salivary secretion and amylase output as well as on amylase gland content. The drugs were infused intravenously for 30 min in the anaesthetized rat. METHODSA total of 53 adult female Sprague-Dawley rats (B &...

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Parasympathetic non-adrenergic, non-cholinergic reflex secretion of parotid acinar granules in rats pretreated with atropine and adrenoceptor antagonists

Cited by 19 publications

References 13 publications

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Depletion of vasoactive intestinal peptide and substance P in parotid glands of atropinized rats during reflex secretion

Acinar degranulation in the rat parotid gland induced by neuropeptides

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