Activation of the Carotid Sinus Nerve After Acute Myocardial Infarction in a Cardiorenal Syndrome Type 1 Model in Sprague–Dawley Rats

ABSTRACT Aim To evaluate the effect of carotid sinus nerve stimulation (CSNS) in the progression of cardiorenal syndrome type 1 (CRS1), 3 days after acute myocardial infarction (AMI). Methods Male rats were divided into four groups. CSNS was applied daily for 10 min over 3 days. Cardiac, renal, and inflammatory parameters characterized the CRS1 and the electroceutical effects of CSNS. Results CSNS reduced the ischemic zone compared to the AMI group not exposed to CSNS (32.7% ± 2.2% vs. 8.0% ± 1.8%). Heart rate (bpm) was increased in the AMI group, showing 440 ± 7.6 at 48 h and 428 ± 1.0 at 60 h post‐AMI. Additionally, arterial pressure (mmHg) was increased in the AMI group at 48 h, as follows: mean: 98 ± 1.7, diastolic: 89 ± 2.1, and systolic: 122 ± 5.3. In contrast, the CSNS + AMI group showed significant reductions of these parameters: mean: 79 ± 2.0, diastolic, 66 ± 1.7, and systolic: 99 ± 2.7. Renal injury was confirmed by increased apoptosis in the AMI group. A significant increase in TNF‐α was observed in both heart and kidneys (pg/mg of tissue) in the AMI group and reduced IL‐6 and IL‐1β levels in the CSNS + AMI group, indicating an attenuation of the inflammatory responses by CSNS. Conclusions This study demonstrates early cardiac and renal dysfunction in CRS1 following AMI, associated with elevated inflammatory markers (TNF‐α, IL‐6, and IL‐1β) and renal apoptosis. Therefore, CSNS appears to be a promising electroceutical approach for CRS1. Besides, on the basis of previous studies from our laboratory, CSNS involves stimulation of the baroreflex, activating the parasympathetic and inhibiting the sympathetic nervous system.