文摘
The interaction between angiotensin [Ang-(1–7)] and bradykinin (BK) was determined in the mesentery of anesthetized Wistar rats using intravital microscopy. Topical application of BK and Ang-(1–7) induced vasodilation that was abolished by the BK B2 receptor antagonist HOE-140 and the Ang-(1–7) antagonist A-779, respectively. BK (1 pmol)-induced vasodilation, but not SNP and ACh responses, was potentiated by Ang-(1–7) 10 pmol and 100 pmols. The effect of 100 pmol of Ang-(1–7) on BK-induced vasodilation was abolished by A-779, indomethacin, and l-nitroarginine methyl esther, whereas losartan was without effect. Enalaprilat treatment enhanced the BK- and Ang-(1–7)-induced vasodilation and the potentiating effect of Ang-(1–7) on BK vasodilation. The potentiation of BK-induced vasodilation by Ang-(1–7) is a receptor-mediated phenomenon dependent on cyclooxygenase-related products and NO release.
