Abstract 1376: Destruction Of Cardiac Sympathetic Afferents Normalizes Sympathoexcitation In Chronic Heart Failure
The enhanced cardiac “sympathetic afferent” reflex has been demonstrated to contribute to increased sympathetic outflow in chronic heart failure (CHF). This is associated with increased angiotensin II in the central nervous system. The rostral ventrolateral medulla (RVLM) has been recognized as a critical area involved in sympathetic outflow. Therefore, the objective of this study was to assess whether inhibition of cardiac sympathetic afferent input decreases sympathetic activity, and if so, whether AT1 receptor mechanisms in the RVLM contribute to this response. The cardiac sympathetic afferents were destroyed by left ventricular epicardial application of resiniferatoxin (RTX, 200 mg) while infraction or sham surgery was performed. The rats were allowed to recover 6 to 8 weeks after surgery. A total of 47 rats were divided into four groups: sham, sham + RTX, CHF, and CHF + RTX. The Table⇓ shows the expression of AT1 receptor protein in the RVLM, the baseline RSNA, and the responses of blood pressure and RSNA to RVLM injection of the AT1 receptor antagonist losartan in the four groups. These results indicate that chronic blockade of the cardiac sympathetic afferent reflex by destruction of cardiac sympathetic afferents normalizes the sympatho-excitation and downregulates the RVLM AT1 receptor in the CHF state, suggesting that tonic cardiac sympathetic afferent input contributes to increased sympathetic activity through the RVLM AT1 receptor mechanism in CHF.