Catecholamine turnover in rats with ventromedial hypothalamic lesions.

Abstract

The disappearance of norepinephrine (NE) from brown adipose tissue, heart, and pancreas in vivo has been examined in rats with ventromedial hypothalamic (VMH) lesions and in appropriate control rats. Two weeks after the introduction of these lesions, the rate of NE turnover following blockade of NE synthesis with alpha-methyl-p-tyrosine was significantly greater in brown adipose tissue and heart of rats with VMH lesions than in sham-operated controls. This significant increase occurred whether the animals were fed ad libitum or pair-gained to the sham-operated controls. In the pancreas, on the other hand, no effects of hypothalamic lesions could be detected. When rats were fasted, NE turnover slowed in both sham-operated and VMH-lesioned rats, but the turnover slowed more in sham-operated than in VMH-lesioned rats. When exposed to the cold for 6 h during measurements of NE turnover, VMH-lesioned rats increased their rate of NE turnover as did sham-operated rats. Fasted animals exposed to the cold had significantly higher rates of NE turnover whether or not they also had VMH lesions. Animals with electrolytic or knife-cut VMH lesions showed comparable rates of NE turnover in the fasted state. Eight weeks after hypothalamic lesions, similar studies were conducted. By this time NE turnover was not significantly different between the VMH-lesioned and sham-operated rats fed ad libitum. However, fasting, which slowed NE turnover in sham-operated rats, had no effect in VMH-lesioned animals. These data are discussed in relation to the autonomic hypothesis.