An insulin-releasing property of imidazoline derivatives is not limited to compounds that block α-adrenoceptors

As we have demonstrated previously phentolamine stimulates the release of additional insulin from isolated mouse islets and raises plasma insulin levels in the whole rat. This effect was independent of the well known property of phentolamine to block alpha-adrenoceptors. In experiments on isolated p...

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Bibliographic Details
Published in:Naunyn-Schmiedeberg's archives of pharmacology 1989-09, Vol.340 (3), p.321-327
Main Authors: SCHULZ, A, HASSELBLATT, A
Format: Article
Language:English
Subjects:
Adrenergic alpha-Antagonists - pharmacology
Animals
Biological and medical sciences
Clonidine - pharmacology
General and cellular metabolism. Vitamins
Glucose - pharmacology
Imidazoles - pharmacology
In Vitro Techniques
insulin
Insulin - metabolism
Islets of Langerhans - drug effects
Islets of Langerhans - metabolism
Male
Medical sciences
Mice
pancreas
Pharmacology. Drug treatments
Phentolamine - pharmacology
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Summary:As we have demonstrated previously phentolamine stimulates the release of additional insulin from isolated mouse islets and raises plasma insulin levels in the whole rat. This effect was independent of the well known property of phentolamine to block alpha-adrenoceptors. In experiments on isolated pancreatic islets from mice we now demonstrate that tolazoline and antazoline which are chemically closely related to phentolamine, share its ability to potentiate insulin release. The following results were taken as evidence that this effect does not result from an alpha-adrenoceptor blocking action of imidazoline compounds. More than 10 times higher concentrations of phentolamine were required to liberate additional insulin from isolated islets than were effective in counteracting the inhibitory effect of clonidine on insulin release. The newly introduced alpha 2-adrenoceptor antagonist BDF 8933, which is an imidazoline derivative, stimulates insulin release as well, while the irreversible alpha-adrenoceptor blocking agent benextramine of different structure failed to do so, even when being present in concentrations blocking the alpha 2-adrenoceptor-mediated effects of clonidine. Antazoline shared the ability of phentolamine to stimulate insulin release despite having no or only very little alpha-adrenoceptor blocking activity. When used under our conditions, it almost entirely failed to alleviate the inhibition of insulin release induced by clonidine. We conclude that the response of the islet cells to imidazoline derivatives is not limited to those capable of blocking alpha-adrenoceptors. On the other hand, alpha-adrenoceptor blocking agents of different chemical structure fail to induce the release of additional insulin.
ISSN:0028-1298
1432-1912
DOI:10.1007/BF00168517