Navegando por Palavras-chave "Receptor B2"
Agora exibindo 1 - 1 de 1
Resultados por página
Opções de Ordenação
- ItemSomente MetadadadosEfeito dos hormônios sexuais no receptor B2 de Cininas(Universidade Federal de São Paulo (UNIFESP), 2021) Arata, Julia Galanakis [UNIFESP]; Pesquero, Joao Bosco [UNIFESP]; Universidade Federal de São PauloHereditary angioedema (HAE) is a rare genetic autosomal dominant disease characterized by attacks of cutaneous and submucosal swelling, which causes weakness and pain to patients and can be life threatening when affecting the upper airways. Edema formation results from vasodilation and vascular permeability increase, in most cases, by the excessive release of bradykinin (BK), due to a disorder in the plasma kallikrein-kinin system. The frequency, severity, and triggers of attacks vary among patients with the disease. In female patients, the action of estrogen (menstruation, pregnancy, and exogenous administration) is reported as an aggravating stimulus for the angioedema attacks. In the present work, we aimed to investigate mechanisms in the kallikrein-kinin system which could be linked to the phenotype difference between women and men with HAE, through in vitro Ca2+ intracellular mobilization assays in endothelial cells transfected with the kinin B2 receptor (B2R), to verify whether the interaction of B2R and its agonist (BK) is influenced by estradiol, testosterone, and attenuated androgens. In our cellular assays, there was no significant effect of these hormones in the intracellular Ca+2 release due to B2R activation by BK that could indicate a possible direct or indirect allosteric regulation by these hormones over the receptor. Estradiol was able to decrease the activity of recombinant angiotensin converting enzyme (ACE) expressed in endothelial cells, although the difference was not significant. These data indicate a possible influence of estrogen on ACE activity, which could reduce BK degradation, and increase AEH severity.