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, 3μg/kg, i.v.) and a depressor dose of sodium nitroprusside (SNP, 30μg/kg, i.v.) before (control) and 5, 15, 30 and 60min after AAC or NAC into the 4thV. Control PHE injection induced baroreflex-mediated bradycardia (−93±13bpm, n=7). Interestingly, after AAC injection into the 4thV, PHE injection produced a transient tachycardia at 5 (40±23bpm), 15 (26±22bpm) and 30min (59±21bpm). No changes were observed in baroreflex-mediated tachycardia evoked by SNP after AAC injection on 4thV (control: 151±23bpm vs. 135±18bpm at 5min after AAC, n=7). In the NAC treated group, PHE induced a reduction in reflex bradycardia at 5min when compared to control (−11±17bpm vs. −83±15bpm, 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.