Effects of inhibitors of nitric oxide synthase on isolated uteri of fasting rats
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 × 10 −6 M); acetyl salicylic acid (10 −4M); 400 μM of N Gmethyl- l-arginine, (L-NMMA) or 400...
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Published in: | Prostaglandins, leukotrienes and essential fatty acids Vol. 59; no. 1; pp. 23 - 26 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
Kidlington
Elsevier Ltd
01-07-1998
Elsevier |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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 × 10
−6 M); acetyl salicylic acid (10
−4M); 400 μM of N
Gmethyl-
l-arginine, (L-NMMA) or 400 μM of sodium nitroprusside (SNP), does not modify the production of
14CO
2 from U
14C-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 methyl ester (L-NAME), or hemoglobin (2 μg ml
−1) a nitric oxide scavenger have the same effects while Nωnitro arginine-
d-methyl ester (D-NAME) does not. However (SNP), a nitric oxide donor, does not alter the production of
14CO
2 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0952-3278 1532-2823 |
DOI: | 10.1016/S0952-3278(98)90048-5 |