Carotid Baroreceptor Magnetic Activation and Beat‐to‐Beat Blood Pressure Variability, Implications to Treat Abrupt Blood Pressure Elevation in Labile Hypertension

Mounting evidence suggests enhanced blood pressure (BP) variability (BPV) independent role in cardiovascular (CV) damage. The goal was to estimate the effect of the carotid baroreceptor (CB) magnetic stimulation on sudden high BP elevation. Mean femoral arterial BP (MAP), heart rate (HR), baroreflex sensitivity (BRS), and ear lobe skin microcirculatory blood flow, by microphotoelectric plethysmography (MPPG), were simultaneously recorded in conscious rabbits sedated by pentobarbital intravenous (i.v.) infusion (5 mg/kg/h) after 40 min CB exposure to 350 mT static magnetic field (SMF), by Nd 2 ‐Fe 14 ‐B magnets ( n = 14), or sham magnets exposure ( n = 14). BRS was assessed from HR and MAP responses to abrupt hypotension induced by i.v. bolus injections of nitroprusside (Ni) and abrupt MAP elevation (MAP AE ) by i.v. bolus of phenylephrine (Ph). Beat‐to‐beat BPV was estimated by MAP standard deviation. SMF CB exposure significantly increased BRS Ni (74.5 ± 17.8%, P < 0.001) and microcirculation (23.8% ± 11.0%, P = 0.039); decreased MAP (−5.7 ± 1.7%, P < 0.014) and phenylephrine‐induced MAP AE (−19.1%, P = 0.043). MAP AE positively correlated with resting MAP ( r = 0.342, P = 0.0383) and MAP SD ( r = 0.383, P = 0.0194), and inversely with BRS Ph ( r = −0.47, P = 0.0156). SMF CB exposure enhanced the nitroprusside, which acts by releasing nitric oxide (NO), vasodilatory effect. This indicates arterial baroreflex to improve vessel sensitivity to NO, which is a new physiology with BP buffering effect. A positive correlation of MAP SD to phenylephrine BP ramps suggests a causal relationship and BPV prognostic significance to forecast abrupt BP elevation. Mechano/baroreceptor magneto‐sensing property proposed to be the basic physiology by which SMFs boost CV autonomic regulation with potential implementation in high CV risk labile arterial hypertensive disease.