Role of the kallikrein–kinin system in Ang-(1-7)-induced vasodilation in mesenteric arterioles of Wistar rats studied in vivo–in situ

• Published in: Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2006-07, Vol.27 (7), p.1770-1775
• Main Authors: Marangoni, Rossana Anderson, Carmona, Adriana Karaoglanovic, Passaglia, Rita Cássia A. Tostes, Nigro, Dorothy, Fortes, Zuleica Bruno, de Carvalho, Maria Helena Catelli
• Format: Article
• Language: English
• Subjects: Angiotensin-(1-7); Animals; Aprotinin - chemistry; Aprotinin - metabolism; Arterioles - metabolism; Biological and medical sciences; Bradykinin; Cysteine - chemistry; Fundamental and applied biological sciences. Psychology; Kallikrein-Kinin System; Kallikreins - chemistry; Male; Microcirculation; Peptidase; Peptide Hydrolases - chemistry; Rats; Rats, Wistar; Renin–angiotensin system; Serine - chemistry; Vasodilation; Vertebrates: endocrinology
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/j.peptides.2006.02.002

Angiotensin-(1-7) [Ang-(1-7)], exerts a variety of actions in the cardiovascular system, with an important effect being vasodilation. In this work, we investigated the relationship between the vasodilatory activity of Ang-(1-7) and the kallikrein–kinin system. Intravital microscopy was used to study the vasodilation caused by Ang-(1-7) in the mesenteric vascular bed of anesthetized Wistar rats. The topical application of Ang-(1-7) caused vasodilation of mesenteric arterioles that was reduced by A-779, JE 049 and peptidase inhibitors (aprotinin, SBTI, PKSI 527, E-64, PMSF). These results indicated that the vasodilation induced by Ang-(1-7) in the mesenteric arterioles of Wistar rats was heavily dependent on the activation of kallikrein and subsequent kinin formation.