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Influence of Cholecystokinin-Receptor Antagonists on Feedback Regulation of Pancreatic Secretion

  • Conference paper
Chronic Pancreatitis

Abstract

In 1981 proglumide and benzotript were shown to act as specific and competitive CCK-receptor antagonists in vitro [32]. However, these compounds had low potencies in antagonizing the action of CCK in the intact organ [62]. More recently, several new CCK antagonists have been described which are more potent in vitro compared to proglumide. First, C-terminal CCK fragments or analogs such as CCK-(27–32)-amide were shown to act as specific CCK antagonists up to 75 times more potent than proglumide [77]. CCK fragments, however, were shown to be rapidly degraded in physiological fluids [45]. Subsequently, peptide molecules with a proglumide-like structure were synthesized which were up to 500–5000 times more potent than proglumide in vitro and in vivo [53, 64–66] (Fig. 1). More recently, asperlicin, a nonpeptide substance isolated from Aspergillus aliaceus (Fig. 1) was shown to act as a specific CCK-antagonist which was 200 times more potent than proglumide in inhibiting CCK-stimulated secretion in vitro [11] (Fig. 2). Asperlicin, however, was poorly water soluble and, thus, difficult to use for in vivo experiments. In 1986, several nonpeptide substances, structurally similar to asperlicin, were described which were more water soluble than asperlicin. The most potent of these asperlicin derivatives, L-364,718, was shown to be 10000 to 3000000 times more potent than proglumide in inhibiting CCK’s action and binding in vitro and in vivo [10, 12, 18, 66] (Figs. 1, 2). Both the new potent peptide and nonpeptide antagonist only inhibit the actions of those agonists which bind to the CCK receptor [66].

C. Niederau was supported by grants from the Deutsche Forschungsgemeinschaft (Ni 224/1–1, 224/2–1, and 224/2–2) and from the Ministerium für Wissenschaft und Forschung des Landes Nordrhein-Westfalen. J.H. Grendell was supported by grants from the Research Evaluation and Allocation Committee, the Committee on Research of the Academic Senate, School of Medicine, University of California, San Francisco, and the National Institute of Health (DK 38939)

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Authors and Affiliations

  1. Medizinische Klinik und Poliklinik, Abteilung für Gastroenterologie, Heinrich-Heine-Universität, Düsseldorf, Germany

    J. H. Grendell

  2. Departments of Medicine and Physiology, University of California, San Francisco, CA, 94143, USA

    J. H. Grendell

  3. Medical Service, San Francisco General Hospital, San Francisco, CA, 94110, USA

    J. H. Grendell

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  1. C. Niederau
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  3. R. Lüthen
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  1. Department of Surgery, University of Ulm, Steinhövelstrasse 9, D-7900, Ulm, W.-Germany

    H. G. Beger M.D.  & M. Büchler M.D.  & 

  2. Department of Internal Medicine II, University of Ulm, Robert-Koch-Strasse 8, D-7900, Ulm, W.-Germany

    H. Ditschuneit M.D.  & P. Malfertheiner M.D.  & 

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Niederau, C., Niederau, M., Lüthen, R., Grendell, J.H. (1990). Influence of Cholecystokinin-Receptor Antagonists on Feedback Regulation of Pancreatic Secretion. In: Beger, H.G., Büchler, M., Ditschuneit, H., Malfertheiner, P. (eds) Chronic Pancreatitis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75319-0_23

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