Abstract Title

Chronic Vagus Nerve Stimulation Attenuates Renal Inflammation in Autoimmune-Induced Hypertension

RAD Assignment Number

320

Presenter Name

Grace Pham

Abstract

Chronic renal inflammation has been implicated in the pathogenesis of hypertension, which identifies the autoimmune disease systemic lupus erythematosus (SLE) as a compelling disease model. The cholinergic anti-inflammatory pathway (CAP) is a vagally mediated neuroimmune pathway that, when impaired, may facilitate the development of chronic inflammation. While stimulation of the CAP attenuates inflammation in various models of inflammatory disease, it is unclear whether the pathway is impaired in SLE, or whether its stimulation is protective. We hypothesized that pharmacological activation of the CAP at the level of the vagus nerve would decrease renal inflammation and therefore blood pressure in a hypertensive SLE mouse model. Initially, female SLE (NZWF1) and control (NZW) mice were administered the efferent vagal stimulant, CNI-1493 (Semapimod hydrochloride; 8 mg/kg IP) or saline twice per week for 4 weeks starting at 30 weeks of age. SLE mice had 1143±439% (p

Presentation Type

Oral

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Chronic Vagus Nerve Stimulation Attenuates Renal Inflammation in Autoimmune-Induced Hypertension

Chronic renal inflammation has been implicated in the pathogenesis of hypertension, which identifies the autoimmune disease systemic lupus erythematosus (SLE) as a compelling disease model. The cholinergic anti-inflammatory pathway (CAP) is a vagally mediated neuroimmune pathway that, when impaired, may facilitate the development of chronic inflammation. While stimulation of the CAP attenuates inflammation in various models of inflammatory disease, it is unclear whether the pathway is impaired in SLE, or whether its stimulation is protective. We hypothesized that pharmacological activation of the CAP at the level of the vagus nerve would decrease renal inflammation and therefore blood pressure in a hypertensive SLE mouse model. Initially, female SLE (NZWF1) and control (NZW) mice were administered the efferent vagal stimulant, CNI-1493 (Semapimod hydrochloride; 8 mg/kg IP) or saline twice per week for 4 weeks starting at 30 weeks of age. SLE mice had 1143±439% (p