Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Castor oil (2 ml orally) produced diarrhoea in rats 1-7 h after challenge, which was associated with gross damage to the duodenal and jejunal mucosa. 2. The injury was accompanied by release of acid phosphatase into the gut lumen, indicating cellular injury. 3. Intraperitoneal injection of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 2.5-50 mg kg-1 twice), prevented the diarrhoea. The dose of L-NAME (50 mg kg-1) completely blocked the diarrhoea but increased the release of acid phosphatase and worsened the gross damage. 4. The NO donating compound, isosorbide-5-mononitrate (IMN, 150 mg kg-1 twice) reversed the effects of L-NAME (50 mg kg-1) on castor oil-induced diarrhoea, gross damage and acid phosphatase release. 5. The apparent dissociation of the diarrhoeal and intestinal mucosal damaging effects of castor oil suggest that NO has a protective effect on the rat duodenal and jejunal mucosa, but that NO mediates, in part, the diarrhoea effect of this laxative.
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PMID:Dissociation of castor oil-induced diarrhoea and intestinal mucosal injury in rat: effect of NG-nitro-L-arginine methyl ester. 788 64

1. The role of endogenous nitric oxide (NO) in adjuvant arthritis in Lewis rats has been studied by use of L-arginine, the amino acid from which NO is synthesized, and NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase. Prolonged modulation (35 days) of the L-arginine: NO pathway in rats was achieved by dissolving test compounds in the drinking water (L-arginine: 3, 10 and 30 mg ml-1; L-NAME: 0.1, 1 and 10 mg ml-1). 2. Arthritis was exacerbated by L-arginine and suppressed by L-NAME in a dose-related fashion. Combined treatment with L-NAME (1 mg ml-1) and L-arginine (30 mg ml-1) did not modify the arthritis. 3. Reduced weight gain, which is a feature of adjuvant arthritis, was modified by these compounds so that L-arginine reduced weight gain whereas L-NAME increased weight gain compared with that in control animals. 4. D-Arginine (30 mg ml-1), NG-nitro-D-arginine methyl ester (D-NAME: 1 mg ml-1) and L-lysine (30 mg ml-1), an amino acid not involved in the generation of NO, were without effect on either arthritis or body weight gain. 5. Antigen-stimulated proliferation of T-lymphocytes as well as generation of nitrite (NO2-) and release of acid phosphatase from macrophages were all enhanced in L-arginine-treated arthritic rats and reduced in L-NAME-treated animals. 6. These results suggest that endogenous NO modulates adjuvant arthritis, possibly by interfering with the activation of T-lymphocytes and/or macrophages.
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PMID:Modulation of adjuvant arthritis by endogenous nitric oxide. 824 42

The modulation of platelet activating factor (PAF) formation in duodenal tissue by nitric oxide (NO) released in response to castor oil was studied in rats pretreated with NG-nitro-L-arginine methyl ester (L-NAME, 6.25-25 mg/kg, i.p.), an inhibitor of NO synthase, NG-nitro-D-arginine methyl ester (D-NAME, 25 mg/kg, i.p.), the inactive enantiomer of L-NAME or isosorbide-5-mononitrate (IMN, 30-90 mg/kg, p.o.), a NO donating compound. Castor oil (2 ml/rat orally) increased PAF production in the rat duodenum 3 h after challenge. L-NAME, but not D-NAME, enhanced the amount of PAF formed by duodenal tissue, while IMN (30-90 mg/kg) counteracted the effects of L-NAME (12.5 mg/kg) and also reduced PAF release in the tissue of rats treated with castor oil. L-NAME 12.5 mg/kg, but not D-NAME, enhanced both macroscopic damage and acid phosphatase release induced by castor oil. These effects were reduced by a PAF antagonist BN 52021 (3-t-Butyl-hexahydro-4, 7b, 11-trihydroxy-8-methyl-9H-1, 7a-epoxymethano-1H, 6aH-cyclopenta [c] furo [2, 3b] furo [3'2':3,4] cyclopenta [1.2-d]furan-5,9,12(4H)trione) 10 and 20 mg/kg i.p. Such findings suggest that endogenous nitric oxide could reduce PAF biosynthesis in castor oil-treated rats.
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PMID:Relationship between nitric oxide and platelet-activating factor in castor-oil induced mucosal injury in the rat duodenum. 873 1

This study was aimed to determine the role of nitric oxide on the skeletal myotoxic activity induced by crotoxin, the major component of the venom of Crotalus durissus terrificus. Rats were treated with N(G)-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase or vehicle for 4 days, and on the 5th day received an intramuscular injection of crotoxin into the tibialis anterior muscle. Rats were also treated with aminoguanidine bicarbonate salt or 7-nitroindazole, inhibitors of the inducible and neuronal isoforms of nitric oxide synthase, respectively, for 4 days and on the 5th day injected with crotoxin. All treated groups were sacrificed 24 h after injection of crotoxin. Tibialis anterior and soleus muscles were removed, frozen and stored in liquid nitrogen. Histological sections were stained with toluidine blue and assayed for acid phosphatase. The results show that L-NAME significantly minimizes myonecrosis induced by crotoxin and both aminoguanidine and 7-nitroindazole partially prevented myonecrosis induced by crotoxin. Based on the present results we conclude that nitric oxide is a very important intracellular signaling molecule that mediates crotoxin myotoxic activity.
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PMID:Role of nitric oxide in myotoxic activity induced by crotoxin in vivo. 1505 6

Treatment with cyclosporin A (CsA) following solid organ transplantations such as heart or liver generally results in bone loss. However, in vitro studies show that CsA inhibits bone resorption. Our previous in vivo animal studies demonstrated that the effects of nitric oxide (NO) on bone are biphasic; at high doses, NO increases bone resorption. In this study, we have examined in an in vitro setting to determine whether the bone loss caused by CsA administration is dependent on the NO-cyclic guanosine monophosphate (cGMP) pathway. Freshly isolated osteoclast-rich neonatal rat long bone marrow cells were added to 100 microM thick dentin sections that had been seeded with neonatal-rat calvarial osteoblasts. These co-cultures were maintained for 48 hrs in a basal medium with CsA (1, 5, and 10 microg/ml), both alone and with either L-Arginine (NO substrate; 10-3M), L-NAME (NO synthase enzyme inhibitor; 10-4M), or the combination of the two. The cultures were then fixed in cold 95% ethanol and stained with tartrate resistant acid phosphatase (TRAP) to identify osteoclasts and sites of osteoclastic resorption. Preparations were analyzed using an automated histomorphometry software package. Scanning electron microscopy affirmed that the areas identified by light microscopy as resorption sites contained osteoclastic lacunae. CsA inhibited bone resorption dose-dependently. CsA at 10 microg/ml produced a 90% inhibition of bone resorption (control = 5.5 -/+2.0%; CsA = 0.64 -/+ 0.09=). L-Arginine reversed this inhibition by 90% (Arg + CsA = 4.23 -/+ 1.57%; CsA = 0.64 -/+ 0.09%). The application of NOS inhibitor L-NAME inhibited bone resorption by 87% (Arg + CsA + L-NAME = 0.55 -/+ 0.14%; Arg + CsA = 4.23 -/+ 1.5%). We conclude that NO-cGMP pathway is involved in the CsA induced bone loss.
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PMID:The mechanism of bone resorption by cyclosporin: involvement of the NO-cGMP pathway. 1575 8

The beneficial health effects of taurine on hypertension have been demonstrated previously in both experimental and epidemiological studies. However, the role of taurine in reproductive dysfunction associated with hypertension has not been investigated. The present study evaluated the therapeutic efficacy of taurine on reproductive deficits in N-nitro-l-arginine methyl ester (L-NAME)-induced hypertensive rats. Sixty male Wistar rats were randomly assigned into six groups namely control, taurine alone, L-NAME alone (40mg/kg) or L-NAME treated with either taurine (100 and 200mg/kg) or reference drug atenolol (10mg/kg) for 28 consecutive days. Results indicated that taurine treatment significantly abrogated L-NAME-induced increase in systolic, diastolic and mean arterial pressures when compared with hypertensive control. Administration of taurine markedly increased antioxidant enzymes activities and glutathione level whereas it suppressed the increase in biomarkers of oxidative stress in the testes and epididymis of L-NAME-induced hypertensive rats. Moreover, taurine significantly reversed hypertension mediated decreases in circulatory concentrations of luteinizing hormone, follicle-stimulating hormone and testosterone whereas it increased testicular sperm number, epididymal sperm number and sperm progressive motility in the hypertensive rats. Furthermore, taurine abrogated the suppression of marker enzymes of testicular function namely acid phosphatase, alkaline phosphatase and lactate dehydrogenase and preserved the histo-architectures of the testes and epididymis in L-NAME-induced hypertensive rats. Taken together, the findings from this study highlight the beneficial role of taurine in reproductive system of L-NAME-induced male hypertensive rats. Taurine supplementation may be a good clinical approach to prevent reproductive deficits in male hypertensive patients.
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PMID:Taurine enhances spermatogenic function and antioxidant defense mechanisms in testes and epididymis of L-NAME-induced hypertensive rats. 2909 64