Noradrenergic mechanisms in brain and peripheral organs after aortic nerve transection

Noradrenergic mechanisms were studied in the hypothalamus, midbrain, medulla, kidney, duodenum, and skeletal muscle of Wistar rats at 3 or 13 days after either bilateral transection of the aortic depressor nerve (ADN) or a sham operation. The rate of decline of tissue norepinephrine (NE) concentration after inhibition of tyrosine hydroxylase with alpha-methyltyrosine was used as an index of NE turnover. Three days after ADN transection, arterial pressure and heart rate were elevated significantly, and NE turnover was increased in all three brain areas, kidney, and skeletal muscle but not in duodenum. The largest change occurred in skeletal muscle, where the time required for tissue NE concentration to decline to 50% of control decreased from 9.0 to 2.5 h. In rats 13 days after ADN transection, arterial pressure was significantly higher than in sham-operated controls, but heart rate was similar to control values. NE turnover was slightly increased in hypothalamus but was not significantly different in muscle and kidney when compared to sham-operated controls. These results suggest that 3 days after ADN transection in the rat, arterial pressure is elevated as a result of increased activity of noradrenergic neurons in the hypothalamus and brain stem, which is translated into increased sympathetic nerve activity to peripheral organs, particularly skeletal muscle. The normal turnover of NE in peripheral organs 13 days after ADN transection suggests that mechanisms other than increased sympathetic activity are responsible for maintaining the elevated arterial pressure.