Key result
Primary activation of kinin receptors by selective B1 or B2 agonists displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases.
Why the study?
Do kinin receptor agonists reduce organ damage in ischemia and diabetes?
Do kinin receptor agonists reduce organ damage in ischemia and diabetes?
Kinin receptor agonists, particularly B1R agonists, show promise in reducing end-organ damage in experimental models of ischemia and diabetes, warranting clinical development.
Hypothesis-generating for kinin agonists in experimental ischemia and diabetes; leaves open clinical translation.
Genetic and pharmacological studies, clinical and experimental, focused on kallikrein-K1, kinin receptors and ACE/kininase II suggest that kinin release in the settings of ischemia or diabetes reduces organ damage, especially in the heart and kidney. Kinin bioavailability may be a limiting factor for efficacy of current kinin-potentiating drugs, like ACE inhibitors. Primary activation of kinin receptors by prototypic pharmacological agonists, peptidase-resistant, selective B1 or B2, displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases. B1R agonism was especially efficient in diabetic animals and had no unwanted effects. Clinical development of kinin receptor agonists may be warranted.
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Desposito et al. (2016) conducted a review in Ischemia and diabetes. Kinin receptor agonists (B1 or B2) was evaluated. Primary activation of kinin receptors by selective B1 or B2 agonists displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases.
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