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Abstract
BackgroundInflammation processes are important participants in the pathophysiology of hypertension and cardiovascular diseases. The role of the alpha7 nicotinic acetylcholine receptor (α7nAChR) in inflammation has recently been identified. Our previous study has demonstrated that the α7nAChR-mediated cholinergic anti-inflammatory pathway is impaired systemically in the genetic model of hypertension. In this work, we investigated the changes of α7nAChR expression in a model of secondary hypertension.MethodsThe 2-kidney 1-clip (2K1C) hypertensive rat model was used. Blood pressure, vagus nerve function, serum tumor necrosis factor-α (TNF-α) and both the mRNA and protein levels of α7nAChR in tissues from heart, kidney and aorta were measured at 4, 8 and 20 weeks after surgery.ResultsCompared with age-matched control, it was found that vagus nerve function was significantly decreased in 2K1C rats with the development of hypertension. Serum levels of TNF-α were greater in 2K1C rats than in age-matched control at 4, 8 and 20 weeks. α7nAChR mRNA in the heart was not altered in 2K1C rats. In the kidney of 2K1C rats, α7nAChR expression was significantly decreased at 8 and 20 weeks, but markedly increased at 4 weeks. α7nAChR mRNA was less in aorta of 2K1C rats than in age-matched control at 4, 8 and 20 weeks. These findings were confirmed at the protein levels of α7nAChR.ConclusionsOur results suggested that secondary hypertension may induce α7nAChR downregulation, and the decreased expression of α7nAChR may contribute to inflammation in 2K1C hypertension.
Highlights
Inflammation processes are important participants in the pathophysiology of hypertension and cardiovascular diseases
Basal arterial pressure and heart rate in 2-kidney 1-clip (2K1C) rats Both Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were significantly increased at 4, 8 and 20 weeks after 2K1C surgery when compared with age-matched sham-operated rats
Vagal tone in 2K1C rats To assess the vagal tone, the cardiovascular effects of atropine were compared between 2K1C and shamoperated rats
Summary
Inflammation processes are important participants in the pathophysiology of hypertension and cardiovascular diseases. The role of the alpha nicotinic acetylcholine receptor (α7nAChR) in inflammation has recently been identified. Our previous study has demonstrated that the α7nAChR-mediated cholinergic anti-inflammatory pathway is impaired systemically in the genetic model of hypertension. The anti-inflammatory actions mediated by either neuronal or nonneuronal cholinergic system are believed to depend on activation of alpha nicotinic acetylcholine receptor (α7nAChR) [11,12,13], and α7nAChR is proposed as an essential regulator of inflammation and a promising pharmacological strategy against infectious and inflammatory diseases [8,14]. If impairment of cholinergic pathways contribute to the development of endorgan damage during hypertension, downregulation of the α7nAChR seems likely
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