Role of the Renin-Angiotensin System, Renal Sympathetic Nerve System, and Oxidative Stress in Chronic Foot Shock-Induced Hypertension in Rats

Abstract

Objective: The renin-angiotensin system (RAS) and renal sympathetic nerve system (RSNS) are involved in the development of hypertension. The present study is designed to explore the possible roles of the RAS and the RSNS in foot shock-induced hypertension.Methods: Male Sprague-Dawley rats were divided into six groups: control, foot shock, RSNS denervation, denervation plus foot shock, Captopril (angiotensin I converting enzyme inhibitor, ACE inhibitor) plus foot shock, and Tempol (superoxide dismutase mimetic) plus foot shock. Rats received foot shock for 14 days. We measured the quantity of thiobarbituric acid reactive substances (TBARS), corticosterone, renin, and angiotensin II (Ang II) in plasma, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and renal noradrenaline content. RAS component mRNA and protein levels were quantified in the cerebral cortex and hypothalamus.Results: The two week foot shock treatment significantly increased systolic blood pressure, which was accompanied by an increase in angiotensinogen, renin, ACE1, and AT1a mRNA and protein expression in the cerebral cortex and hypothalamus, an increase of the plasma concentrations of renin, Ang II, corticosterone, and TBARS, as well as a decrease in plasma SOD and GSH-Px activities. Systolic blood pressure increase was suppressed by denervation of the RSNS or treatment with Captopril or Tempol. Interestingly, denervation or Tempol treatment both decreased main RAS components not only in the circulatory system, but also in the central nervous system. In addition, decreased antioxidant levels and increased TBARS and corticosterone levels were also partially restored by denervation or treatment with Tempol or Captopril.Conclusions: RAS, RSNS and oxidative stress reciprocally potentiate to play important roles in the development of foot shock-induced hypertension.

HMGB1/RAGE axis mediates stress-induced RVLM neuroinflammation in mice via impairing mitophagy flux in microglia

“…Their in vitro data further revealed that infrasound directly induced microglial activation and upregulated their CRH-R1 expression, which suggests that in addition to the neurons, microglial cells are the effector cells for the infrasound-induced stress as well. Dong et al [49] and Wang et al [50] reported that the 2-week foot shock treatment significantly increased SBP. Our modified method used a series of foot electric shocks synchronous with noise stimulation for 15 days to create a model of stress-related hypertension [24].…”

Angiotensin 1-7 administration alters baroreflex sensitivity and renal function in sympathectomized rats

“…It was reported that renal sympathetic nerves and RAS have reciprocal interaction (6). RAS components alter the renal sympathetic nerve activity (RSNA) (7).…”

Effects of Extracts from Tiaozhi Granule and Its Components on Expression of Scavenger Receptor Class B Type I

“…SR-BI mRNA expression was measured by RT-PCR as previously described [19]. In brief, total RNA was isolated from cells by guanidinium isothiocyanate-acid phenol extraction.…”

“…Expressions of SR-BI protein were measured by western blotting as our previous report [19]. Briefly, cells were harvested and lysates were resolved by 10% SDS-PAGE.…”