Nicotine reduces blood pressure in mouse model of systemic lupus erythematosus

Abstract

Stimulation of the cholinergic anti‐inflammatory pathway through nicotinic acetylcholine receptors (α7nAchR) can suppress systemic inflammation by a mechanism involving vagus nerve activation. Evidence supports an important role for immune system activation and inflammation in the pathogenesis of hypertension. Hypertension and renal injury are prevalent in human patients with the chronic autoimmune inflammatory disorder, systemic lupus erythematosus (SLE), and some evidence suggests that these patients have impaired vagal function. Based on this, we hypothesized that the cholinergic anti‐inflammatory pathway is impaired in SLE and that activation of the pathway via nicotine would reduce blood pressure in mice with SLE. Female SLE (NZBWF1) and control (NZW) mice were infused with nicotine or vehicle for 7 days (2 mg/kg subcutaneous) after which time blood pressure was assessed. Blood pressure (mmHg) was higher in vehicle‐treated SLE mice compared to controls (135±7 vs. 114±4). Blood pressure in nicotine‐treated SLE (119±9) and control (114±1) mice was similar to vehicle‐treated controls. These data implicate impairment of the cholinergic anti‐inflammatory pathway in the development of SLE‐associated hypertension and suggest that it may be an important pathway to target clinically in patients with chronic inflammatory diseases associated with hypertension. AHA4350019, 5T32HL10532, HL051971