The effects of inhibitors of nitric oxide synthase on the glucose metabolism of uteri isolated from 4-day underfed rats were studied. In control rats receiving normal feeding, the addition of indomethacin (5 x 10-6 M); acetyl salicylic acid (10-4M); 400 μM of N(G)methyl-L-arginine, (L-NMMA) or 400 μM of sodium nitroprusside (SNP), does not modify the production of 14CO2 from U14C-glucose. On the contrary, in fasted rat uteri, indomethacin increases glucose oxidation significantly, while acetyl salicylic acid does not alter it. Also, the addition of L-NMMA has no effect. In another group of experiments, in the preparations containing indomethacin of uteri isolated from underfed rats, the addition of L-NMMA significantly changes the effect of indomethacin. Another inhibitor of nitric oxide synthase, Nωnitro-L-arginine-D-methyl ester (L-NAME), or hemoglobin (2 μg ml-1) a nitric oxide scavenger have the same effects while Nωnitro-L-arginine-D-methyl ester (D-NAME) does not. However (SNP), a nitric oxide donor, does not alter the production of 14CO2 in uteri isolated from fasted rats. These results show that in underfed rats, indomethacin increases glucose oxidation independently from its inhibiting effect on cyclooxygenase. Specific inhibitors of nitric oxide synthase can reverse this effect.
|Original language||English (US)|
|Number of pages||4|
|Journal||Prostaglandins Leukotrienes and Essential Fatty Acids|
|State||Published - Jul 1998|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology