Central antioxidant therapy inhibits parasympathetic baroreflex control in conscious rats.

Abstract

Baroreceptor reflex is an important system for neural control of blood pressure. Recently, reactive oxygen species (ROS) have been shown to play an important role in neuronal activity of central areas related to blood pressure control. The aim of this study was to investigate the effects elicited by ascorbic acid (AAC) and N-acetylcysteine (NAC) injections into the 4thV on the parasympathetic component of the baroreflex. Male Wistar rats were implanted with a stainless steel guide cannula into the 4thV. One day prior to the experiments, the femoral artery and vein were cannulated for pulsatile arterial pressure, mean arterial pressure and heart rate measurements and drug administration, respectively. After baseline recordings, the baroreflex was tested with a pressor dose of phenylephrine (PHE, 3_g/kg, i.v.) and a depressor dose of sodium nitroprusside (SNP, 30_g/kg, i.v.) before (control) and 5, 15, 30 and 60 min after AACorNACinto the 4thV. ControlPHEinjection induced baroreflex-mediated bradycardia (−93±13 bpm, n = 7). Interestingly, after AAC injection into the 4thV, PHE injection produced a transient tachycardia at 5 (40±23 bpm), 15 (26±22 bpm) and 30 min (59±21 bpm). No changes were observed in baroreflexmediated tachycardia evoked by SNP after AAC injection on 4thV (control: 151±23bpm vs. 135±18bpm at 5 min after AAC, n = 7). In the NAC treated group, PHE induced a reduction in reflex bradycardia at 5 min when compared to control (−11±17bpm vs. −83±15 bpm, n = 7). No changes were observed in baroreflex-mediated tachycardia evoked by SNP after NAC injection on 4thV. The antioxidants AAC and NAC may act in the central nervous system affecting the parasympathetic component of the cardiac baroreflex.