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Aliskiren associate with L‐arginine improves aorta vascular reactivity of renovascular hypertension rats (867.9)
Author(s) -
Santuzzi Cintia Helena,
Tiradentes Renata,
Mengal Vinicius,
Gouvea Sonia,
Abreu Glaucia
Publication year - 2014
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.28.1_supplement.867.9
Subject(s) - phenylephrine , aliskiren , medicine , endocrinology , sodium nitroprusside , nitric oxide , renovascular hypertension , nitric oxide synthase , arginine , chemistry , losartan , aorta , blood pressure , renin–angiotensin system , biochemistry , amino acid
We evaluate the effects of aliskiren + L‐arginine on the vascular reactivity and systolic blood pressure (SBP) in aortic rings in renovascular hypertensive rats. Animals were randomly assigned to one of five groups: sham, 2 kidney one clip hypertension (2K1C), 2K1C treated with aliskiren (ALSK), 2K1C treated with L‐arginine (L‐arg), and 2K1C treated with aliskiren plus L‐arginine (ALSK+ L‐arg). All Treatments were started 7 days after 2K1C hypertension and the treatments were conducted for 21 days: 2K1C had the following effects: increase in SBP; increased of contractile response to phenylephrine (1 nM‐100 mM) of aortic rings; impairment of the relaxation induced by acetylcholine (0.1 nM‐300 mM) and unaffected relaxation induced by sodium nitroprusside (0.01 nM‐0.3 mM). The treatment with ALSK+L‐arg was able to decreased the contractile response to phenylephrine and improve the acetylcholine relaxation. Endothelium removal and NG‐nitro‐L‐arginine methyl ester (100 mM) increased the response to phenylephrine in 2K1C rats more than in ALSK+L‐arg treated group rats. Losartan (10 mM) reduced the response to phenylephrine in all groups and enalapril (10 mM) reduced the response only in 2K1C and ALSK groups. The endothelial nitric oxide synthase expression increased in 2K1C and L‐arg group, inducible nitric oxide synthase increased only in 2K1C group, neuronal nitric oxide synthase increased in L‐arg and ALSK+L‐arg group and AT1 expression increased in 2K1C and L‐arg group and AT2 expression increased only in ALSK+L‐arg, but no difference found in ACE expression. Results suggest that ALSK+L‐arg treatment promoted the preservation of aortic endothelial function and this can be one of the factors that contributed to the normalization of SBP in this group, furthermore, these data suggest an important modulation of the renin‐angiotensin system associated with direct effects of L‐arginine to enhance vasodilation and modulate the protein expression of nitric oxide synthase in aorta of 2K1C rats.