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Cardiovascular effects of Angiotensin peptides are differentially mediated at the CVLM of hypertensive rats
Author(s) -
Sousa Graziele G,
Castro Uberdan GM,
Silva Marcelo E,
Santos Robson AS,
Campagnole-Santos MariaJose,
Alzamora Andreia C
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.891.21
Subject(s) - microinjection , medicine , endocrinology , renovascular hypertension , angiotensin ii , medulla , renin–angiotensin system , blood pressure , nitric oxide , chemistry
In the present study we investigated the effect of the non‐selective nitric oxide (NO) synthase inhibitor, L‐NAME, or the antioxidant vitamin C (Vit C) on the cardiovascular effects triggered by angiotensin (Ang) II and Ang‐(1–7) at the caudal ventrolateral medulla (CVLM) of renovascular hypertensive rats (2K1C). CVLM microinjection of L‐Name induced similar fall in blood pressure in Sham or 2K1C, while Vit C produced a fall in BP (− 19±4 mmHg, n=5) only in 2K1C rats. L‐NAME did not alter the hypotensive effect induced by CVLM microinjection of Ang II in Sham or 2K1C. However, L‐NAME increased the hypotensive effect of Ang‐(1–7) in Sham and did not alter its effect in 2K1C. In contrast, Vit C abolished the hypotensive effect of Ang II in the CVLM of both groups and did not change the hypotensive effect of Ang‐(1–7) in the CVLM of 2K1C (−12±1 mmHg, n=6) or Sham (− 12±1 mmHg, n=5). These data suggest that different mechanisms are involved in the cardiovascular effects of Ang peptides at the CVLM. Further, our results suggest that part of these mechanisms may be impaired in 2K1C hypertension.