1983
DOI: 10.1111/j.1476-5381.1983.tb09412.x
|View full text |Cite
|
Sign up to set email alerts
|

The role of nicotinic receptors in dog pancreatic exocrine secretion

Abstract: The effects of pentamethonium, an autonomic ganglion blocker, were studied on the exocrine pancreatic secretion of six conscious dogs given intravenous infusions of urecholine, caerulein or pentagastrin on a background of submaximal doses of secretin. 2 Urecholine-induced protein secretion was not affected but both caerulein-and to a smaller extent, pentagastrin-induced protein secretions were depressed by pentamethonium. 3 These results indicate that intravenous caerulein and pentagastrin, but not urecholine,… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

1
2
0

Year Published

1984
1984
2016
2016

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(3 citation statements)
references
References 17 publications
1
2
0
Order By: Relevance
“…M3 receptors are also located on insulin-secreting islet cells; however, in the present study, the carbachol-stimulated amylase secretion was not influenced by diazoxide, suggesting that carbachol activation of the acinar cell muscarinic receptors was dominant. In contrast, caerulein, at concentrations comparable to physiological concentrations of CCK, has been postulated to stimulate amylase secretion via mechanisms including CCK-1 receptors (18), atropine-sensitive neural pathways (21,46), and nicotinic receptors (11). Our findings that caerulein-stimulated amylase secretion is completely abrogated by atropine and tetrodotoxin confirms previous reports that the effect of caerulein on pancreatic exocrine secretion is mediated through cholinergic neural pathways (21,46).…”
Section: Discussionsupporting
confidence: 90%
“…M3 receptors are also located on insulin-secreting islet cells; however, in the present study, the carbachol-stimulated amylase secretion was not influenced by diazoxide, suggesting that carbachol activation of the acinar cell muscarinic receptors was dominant. In contrast, caerulein, at concentrations comparable to physiological concentrations of CCK, has been postulated to stimulate amylase secretion via mechanisms including CCK-1 receptors (18), atropine-sensitive neural pathways (21,46), and nicotinic receptors (11). Our findings that caerulein-stimulated amylase secretion is completely abrogated by atropine and tetrodotoxin confirms previous reports that the effect of caerulein on pancreatic exocrine secretion is mediated through cholinergic neural pathways (21,46).…”
Section: Discussionsupporting
confidence: 90%
“…In the experimental setting, caerulein (an octapeptide analogue of CCK) has been shown to stimulate exocrine secretion at least in part by nicotinic receptors at concentrations comparable to physiological concentrations of CCK [55]. In the early 90s, Chowdhury et al [24] in their murine experiments had noted that nicotine in high doses over 16 weeks resulted in functional as well as morphological changes in the exocrine pancreas.…”
Section: The Exocrine Pancreasmentioning
confidence: 98%
“…The action of atropine was to shift the peak curve to the nadir one. A further shift by hexamethonium indicates the importance of nicotinic mechanisms (Hong & Magee, 1970;Devaux, Diaz, Kubota, Magee & Sarles, 1983 (Fig. 5 and Table 1)).…”
Section: Resultsmentioning
confidence: 99%