Home General Physiology and Biophysics 2013 General Physiology and Biophysics Vol.32, No.4, p.569-575, 2013

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Founded: 1982
ISSN  1338-4325 (online)

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General Physiology and Biophysics Vol.32, No.4, p.569-575, 2013

Title: Physiological regulation of pro-inflammatory cytokines expression in rat cardiovascular tissues by sympathetic nervous system and angiotensin II
Author: Houcine Dab, Rafik Hachani, Mohsen Sakly, Giampiero Bricca, Kamel Kacem


Pro-inflammatory cytokines regulation by sympathetic nervous system (SNS) and angiotensin II (ANG II) was widely described in cardiovascular system, but the role of such neuro-humoral interaction needs further investigation in this context.
We tested SNS-ANG II interaction on IL-6 and TNF-α mRNA expression in left ventricle (LV) and aorta from normotensive rats by sympathectomy with guanethidine and blockade of the ANG II AT1 receptors (AT1R) antagonist with losartan. mRNA synthesis of IL-6 and TNF-α were performed by Q-RT-PCR.

In the LV, IL-6 mRNA increased by 63% (p< 0.01) after sympathectomy, still unchanged after losartan treatment and decreased by 38% (p<0.05) after combined treatment.

TNF-α mRNA decreased by 44% (p< 0.01), only after combined treatment.

In the aorta, IL-6 mRNA increased equally by 65% (p<0.05) after sympathectomy or losartan treatment.

TNF-α mRNA decreased respectively by 28, 41, and 42% (p<0.05) after sympathectomy, losartan and combined treatments.

Our data suggest that ANG II stimulates directly (via AT1R) and indirectly (via SNS) IL-6 mRNA synthesis in LV and aorta and TNF-α mRNA in LV. ANG II seems unable to influence directly TNF-α mRNA synthesis in the aorta but can stimulate this cytokine via SNS. The results are relevant to prevent or reduce proinflammatory cytokines overexpression seen in cardiovascular diseases.

Keywords: Sympathectomy — Angiotensin II AT1 receptor antagonist — IL-6 — TNF-α — Left ventricle — Aorta
Published online: 02-Aug-2013
Year: 2013, Volume: 32, Issue: 4 Page From: 569, Page To: 575

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