Our aim was to examine the modulatory effect of electrical activation (EA) of the carotid baroreflex upon the inflammatory responses elicited by LPS. Wistar rats were divided into 3 groups: 1) Control (Saline); 2) LPS; 3) LPS + EA. The subjects were implanted with electrodes around the carotid sinus and catheters into the femoral artery and jugular vein. The surgical procedures were performed under ketamine/xylazine anesthesia. On the next day, the arterial pressure (AP) and heart rate (HR) were recorded, in conscious rats, followed by saline or LPS (1.5 mg/kg iv) administration combined with EA (1mA; 1ms; 30Hz) of the carotid sinus for 1h. Plasma was collected 1, 2 and 3 hs after saline or LPS administration, while the spleen and the heart were collected after 3 hours, to quantify interleukin 6 (IL‐6), 10 (IL‐10), 1β (IL‐1β) and tumor necrosis factor (TNFα). EA did not change the AP or HR, but reduced (LPS vs LPS+EA) inflammatory cytokine TNF‐α (283±139 vs 115±72 pg/µL at the1st h), IL‐6 (11310±1521 vs 3397±709 pg/µL at the 3rd hour) and IL‐1β (296±24 vs 107±29 pg/µL at the1st h), while increased anti‐inflammatory cytokine IL‐10 (25±9 vs 83±25 pg/µL at the 3rd hour). EA reduced IL‐1β (1.66±0.44 vs 1.24±0.14 pg/µg of protein) and increased IL‐10 (0.89±0.08 vs 1.12±0.05 pg/µg of protein) in the spleen, while reduced the IL‐6 (6.43±1 vs 2.88±0.42 pg/µg of protein) and increased IL‐10 (0.8±0.1 vs 1.05±0.14 pg/µg of protein) in the heart. We concluded that electrical activation of the carotid baroreflex, in conscious rats, reduced pro‐inflammatory and increased anti‐inflammatory cytokines, modulating the inflammatory response elicited by LPS.Financial Support: FAPESP, CAPES and CNPq.

Electrical stimulation (ES) of the carotid sinus (CS) has been used to treat resistant arterial hypertension. Our aim was to evaluate, in conscious normotensive and spontaneously hypertensive rats (SHR), the effect of sustained (60 min) ES of CS on arterial pressure (AP), heart rate (HR) and heart rate variability (HRV). Male Wistar rats (n=8) and SHR (n=8) had the left CS surrounded by a pair of electrodes and insulated from adjacent tissues. A catheter was introduced into the femoral artery and exteriorized together with the CS electrodes. On the next day, conscious rats under continuous recording of AP had their CS stimulated with square pulses of 1 mA, 1 ms, and 30 Hz, delivered randomly, continuously or intermittently (20/20 s ON/OFF), during 60 min. On the following day the type of CS stimulation was inverted. To analyze HRV, segments of 5 min were selected immediately before, at the onset, middle and end of ES period. Greater sustained fall in AP due to ES of CS was observed in SHR (‐50±7 vs ‐11±2 mmHg). A conspicuous bradycardia was also elicited by sustained ES of the CS (‐62±15 and ‐32±11 bpm in SHR and Wistar rats). No difference was observed between continuous or intermittent ES of CS. Overall, HRV was increased by ES of CS only in SHR (from 4.8±0.6 to 11.7±3.2, 7.0±0.6 and 6.7±1.0 bpm at the onset, middle and end of ES). Surprisingly, no differences were observed in HR spectra during ES of CS in both groups. We conclude that ES of the CS was more effective to reduce AP and HR in SHR as compared to normotensive rats. Moreover, despite a marked effect of ES in overall HRV in SHR, no changes in HR spectra were observed.Financial Support: FAPESP, CAPES and CNPq.