Hemodynamic effect produced by microinjection of angiotensins at the caudal ventrolateral medulla of spontaneously hypertensive rats.

• Autor(a) principal: Ferreira, Patrícia Maria
• Data de Publicação: 2008
• Outros Autores: Alzamora, Andréia Carvalho, Santos, Robson Augusto Souza dos, Santos, Maria José Campagnole dos
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFOP
• Texto Completo: http://www.repositorio.ufop.br/handle/123456789/1106
• topic: Caudal ventrolateral medulla; Arterial pressure; Vascular blood flow; Spontaneously hypertensive rats

In the present study, the effect of caudal ventro-lateral medulla (CVLM) microinjection of angiotensin-(1-7) (Ang-(1-7)) and angiotensin II (Ang II) on mean arterial pres-sure (MAP), heart rate (HR) and pulsatile vascular blood flow (VBF; Transonic System) of the femoral, renal or mesenteric arteries was evaluated in male Wistar and spontaneously hypertensive rats (SHR) anesthetized with urethane. The vas-cular resistance (VR) was calculated by the ratio between the changes in MAP and VBF. Ang-(1-7) (40 ng) and Ang II (40 ng) microinjection into the CVLM caused similar depressor ef-fects in Wistar rats and SHR. The hypotensive effect pro-duced by Ang-(1-7) into the CVLM of Wistar rats was accom-panied by a decrease in femoral ( VR/VRbaseline 0.12 0.04 vs. 0.001 0.03; after saline) and renal ( VR/VRbase-line 0.10 0.02 vs. 0.003 0.02; after saline) vascular re-sistance. On the other hand, the Ang II hypotensive effect in Wistar rats produced only changes in renal vascular resis-tance ( VR/VRbaseline 0.16 0.02 vs. 0.003 0.02; after saline). In SHR, the hypotensive effect produced by Ang-(1-7) and Ang II caused decrease in renal vascular resistance ( VR/VRbaseline 0.18 0.03 and 0.13 0.01, respectively, as compared with saline, VR/VRbaseline 0.06 0.02), but did not alter the femoral or mesenteric vascular resistance. These data show that Ang II and Ang-(1-7) hypotensive effect at the CVLM involves the participation of different vascular beds. Further, the lack of involvement of the femoral vascular bed in SHR suggests that hypertension may induce alteration in the neural control of the different vascular beds, at least at the CVLM.