CHANGES IN EATING BEHAVIOR AND THERMOGENIC ACTIVITY FOLLOWING INHIBITION OF NITRIC-OXIDE FORMATION

The effects of the inhibition of nitric oxide (NO) production on eating behavior and thermogenesis were evaluated in the present experiments. N-G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO production, was injected intraperitoneally or intracerebroventricularly, and food intake, oxygen consumption rate, and interscapular brown adipose tissue (BAT) temperature were evaluated in conscious rats. The firing rate of sympathetic nerves innervating interscapular BAT was recorded in urethan-anesthetized animals. L-NAME, intraperitoneally injected, decreased food intake, oxygen consumption, temperature, and firing rate of sympathetic nerves innervating interscapular BAT. Intracerebroventricular injection of L-NAME decreased food intake and enhanced oxygen consumption, temperature, and firing rate of sympathetic nerves innervating BAT. The latter changes were similar to those found after lateral hypothalamic lesions. The opposite changes in oxygen consumption, temperature, and sympathetic activity of BAT that followed L-NAME injection through the two different routes were probably due to different effects of the molecule on sympathetic output. Impaired brain production of NO, which followed intracerebroventricular L-NAME, directly increased sympathetic activity, whereas the same activity that followed intraperitoneal L-NAME was depressed by increased blood pressure, which was elicited by the impaired peripheral production of NO.