Does insulin release kinins in rats?

Rat uterus maintained in situ was used as a bioassay of kinins possibly released in vivo by hyperglycaemia or insulin. Intravenous injections of bradykinin induced contractions of rat uterus which were suppressed by HOE 140, a bradykinin B 2 receptor antagonist. Des-Arg 9-bradykinin, a kinin B 1 rec...

Full description

Saved in:
Bibliographic Details
Published inEuropean journal of pharmacology Vol. 525; no. 1; pp. 154 - 160
Main Authors Damas, Jacques, Garbacki, Nancy, Lefèbvre, Pierre J.
Format Journal Article Web Resource
LanguageEnglish
Published Amsterdam Elsevier B.V 21.11.2005
Elsevier
Elsevier Science Bv
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Rat uterus maintained in situ was used as a bioassay of kinins possibly released in vivo by hyperglycaemia or insulin. Intravenous injections of bradykinin induced contractions of rat uterus which were suppressed by HOE 140, a bradykinin B 2 receptor antagonist. Des-Arg 9-bradykinin, a kinin B 1 receptor agonist, did not elicit any response. After propranolol, the effects of bradykinin were enhanced and dose-dependent. This potentiation did not appear in adrenalectomized rats. Captopril, an angiotensin-converting enzyme (ACE) inhibitor, largely increased the effects of bradykinin. In animals pretreated with propranolol, captopril and atosiban, an oxytocin antagonist, intravenous infusion of glucose induced hyperglycaemia and after a delay increased the uterine contractile activity. This contractile effect of glucose was abolished by HOE 140. Infusion of insulin with glucose induced contractions of the uterus. These responses did not appear or were suppressed by HOE 140 or by soya bean trypsin inhibitor (SBTI), a plasma kallikrein inhibitor. These results are direct evidence that insulin induces a release of kinins.
Bibliography:scopus-id:2-s2.0-28044464957
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2005.10.001