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Kinins are potent vasoactive peptides generated in blood and tissues by the kallikrein serine proteases. Two distinct kinin receptors have been described, one constitutive (subtype B 2 ) and one inducible (subtype B 1 ), and many physiological functions have been attributed to these receptors, including glucose homeostasis and control of vascular permeability. In this study we show that mice lacking the kinin B 1  receptor (B 1  -/-  mice) have lower fasting plasma glucose concentrations but exhibit higher glycemia after feeding when compared to wild-type mice. B 1  -/-  mice also present pancreas abnormalities, characterized by fewer pancreatic islets and lower insulin content, which leads to hypoinsulinemia and reduced insulin release after a glucose load. Nevertheless, an insulin tolerance test indicated higher sensitivity in B 1  -/-  mice. In line with this phenotype, pancreatic vascular permeability was shown to be reduced in B 1  receptor-ablated mice. The B 1  agonist desArg 9 bradykinin injected intravenously can induce the release of insulin into serum, and this effect was not observed in the B 1  -/-  mice or in isolated islets. Our data demonstrate the importance of the kinin B 1  receptor in the control of pancreatic vascular homeostasis and insulin release, highlighting a new role for this receptor in the pathogenesis of diabetes and related diseases.

Role of the kinin B 1 receptor in insulin homeostasis and pancreatic islet function