Acute homocysteine administration does not elevate sympathetic nerve activity in rats.

Both hyperhomocystenemia and sympathetic overactivity are characterized by increased platelet aggregation, proliferation of vascular smooth muscle, accelerated atherosclerosis, left ventricular hypertrophy, and arterial hypertension. This coexistence of pathophysiological features suggests the possibility that homocysteine may cause increases in sympathetic nerve activity (SNA), which may in turn contribute to vascular and end-organ damage. To test this, we gave continuous intravenous infusion of vehicle (saline) in control experiments, or d,l-homocysteine (2.5 mg/kg, followed by 10 mg/ml at 4 ml/(hkg)) in urethane anesthetized rats while measuring mean arterial pressure, heart rate, and lumbar SNA. We found that a 105 min infusion of homocysteine had no significant effect on lumbar sympathetic outflow. In addition, there was no effect of acute homocysteine on heart rate or blood pressure. These findings indicate that acute administration of homocysteine does not increase the firing rate of the lumbar sympathetic nerves in anesthetized rats.