Evidence for the direct action of gastrin-releasing peptide(GRP) on amylase secretion from rat pancreatic acini. An assessment using a perifusion system.

Abstract

We examined the effects of porcine gastrin-releasing peptide (GRP) on exocrine secretion from dispersed rat pancreatic acini using a perifusion system. GRP stimulated amylase secretion, in a dose-dependent manner in the range of 10-10-10-5 M. The submaximum response was observed at 10-8 M. Stimulation with 10-8 M GRP caused a biphasic release of amylase. Amylase secretion by GRP stimulation was not affected by the addition of carbachol, dibutyryl cyclic GMP, or atropine. W-7, a calmodulin antagonist, inhibited the amylase secretion induced by GRP. The addition of isobutylmethylxanthine or secretin increased amylase secretion caused by GRP stimulation. These observations suggest that GRP facilitates enzyme secretion by a direct action on pancreatic acini and not through muscarinic and cholecystokinin receptors. The interaction by the Cat +-calmodulin complex was suggested.

The inhibitory effect of CR-1409 on amylase secretion and intracellular Ca2+ mobilization in rat pancreatic acini in vitro.

“…Cell viability, assessed by the trypan blue exclusion test, was not affected by the loading of fura-2/AM. Secretagogues were used at the submaximal concentrations determined previously (IMAMURA et al, 1983;SHINOZAKI et al, 1986;SHINOZAKI and FUNAKOSHI, 1988 …”

Lack of appropriate citation

“…3 In OLETF rats, two exons were deleted indicating a congenital defect of gene expression of the CCK-A receptor. 4,5 We have proposed that OLETF rats could be a useful experimental model for examining the biological functions of the CCK-A receptor, as so-called "naturally occurring CCK-A receptor gene knockout rats." Therefore, concerning the genetic abnormality of CCK-A receptor in OLETF rats, the lack of citation of our previous publications (especially reference 2) in the study of Nakamura et al 1 might cause misunderstanding.…”

“…This would appear to be a case of inappropriate citation of an article that has not been accepted. Moreover, the above-mentioned Occupational and Environmental Health, Japan, School of Medicine, 1-1 Iseigaoka, Yahatanishi-ku, Kirakyushu 807-8555, Japan article by Funakoshi and his group 1 cited only their own publications for the isolation of rat pancreatic acini, 5,6 which could well give the mistaken impression that they had developed the methods, without acknowledging in any way the original publications by Amsterdam and Jamiesion. 7,8 Since this seemed to be a typical case of lack of appropriate citations and inappropriate citations, 1,2 we did not cite the "in press" articles but nevertheless acknowledged the work of Funakoshi and his group by citing their first paper about OLETF rats.…”

Down‐regulation of bombesin binding to guinea‐pig pancreatic acinar cells during homologous desensitization

“…The signal generated by interaction with the acinar cell receptor for bombesin (Jensen et al, 1978;Zhu et al, 1991) is at least partially transduced by lysis of polyphosphoinositides leading to formation of Ca2" mobilizing inositol 1,4,5-tris-phosphate and protein kinase C activating diacylglycerol (Pandol et al, 1985;Sjodin et al, 1990;Matozaki et al, 1991). Interaction with the receptor induces amylase secretion which exhibits a relatively rapid tachyphylaxis both in vitro (Shinozaki & Funakoshi, 1988) and in vivo (Coy et al, 1992).…”