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Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats.
Liver Int. 2005 Feb; 25(1):131-40.LI

Abstract

Nitric oxide (NO) has been implicated in cirrhosis and might be implicated in renal failure end-stage cirrhosis.

AIM

Our aim was to evaluate NO role in renal failure induced during decompensated cirrhosis, using the following inhibitors: aminoguanidine (AG), a specific inducible nitric oxide synthase (iNOS) inhibitor and NG-nitro-l-arginine methyl ester (L-NAME), a nonselective blocker of NOS isoforms.

METHODS

Endothelial (eNOS) and iNOS gene expression was analyzed by reverse transcriptase-polymerase chain reaction. Cirrhotic rats received a single intragastric dose of CCl(4) to induce acute liver damage (ALD).

RESULTS

After ALD, aspartate aminotransferase highest levels were observed in rats treated with AG and ALT in rats treated with L-NAME. Inhibitors decreased creatinine serum levels to normal values and serum sodium levels re-established after the third day of ALD. L-NAME diminished (P<0.05) eNOS RNA renal expression. Renal iNOS with no inhibitor was overexpressed but was down-regulated by AG treatment. Liver eNOS RNA expression had a decreased expression before ALD in cirrhotic rats, but L-NAME treatment down-regulated eNOS after ALD. AG induced an important iNOS liver decrease.

CONCLUSION

Both inhibitors improved renal function, although AG displayed a better effect and did not aggravate liver function. We concluded that NOS isoforms are implicated in the renal pathophysiologic events induced by ALD.

Authors+Show Affiliations

Instituto de Biología Molecular en Medicina y Terapia Génica. C.U.C.S. U. de G, Mexico, Mexico.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15698410

Citation

Islas-Carbajal, M C., et al. "Nitric Oxide Synthases Inhibition Results in Renal Failure Improvement in Cirrhotic Rats." Liver International : Official Journal of the International Association for the Study of the Liver, vol. 25, no. 1, 2005, pp. 131-40.
Islas-Carbajal MC, Covarrubias A, Grijalva G, et al. Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats. Liver Int. 2005;25(1):131-40.
Islas-Carbajal, M. C., Covarrubias, A., Grijalva, G., Alvarez-Rodríguez, A., Armendáriz-Borunda, J., & Rincón-Sánchez, A. R. (2005). Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats. Liver International : Official Journal of the International Association for the Study of the Liver, 25(1), 131-40.
Islas-Carbajal MC, et al. Nitric Oxide Synthases Inhibition Results in Renal Failure Improvement in Cirrhotic Rats. Liver Int. 2005;25(1):131-40. PubMed PMID: 15698410.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats. AU - Islas-Carbajal,M C, AU - Covarrubias,A, AU - Grijalva,G, AU - Alvarez-Rodríguez,A, AU - Armendáriz-Borunda,J, AU - Rincón-Sánchez,A R, PY - 2005/2/9/pubmed PY - 2005/5/27/medline PY - 2005/2/9/entrez SP - 131 EP - 40 JF - Liver international : official journal of the International Association for the Study of the Liver JO - Liver Int VL - 25 IS - 1 N2 - UNLABELLED: Nitric oxide (NO) has been implicated in cirrhosis and might be implicated in renal failure end-stage cirrhosis. AIM: Our aim was to evaluate NO role in renal failure induced during decompensated cirrhosis, using the following inhibitors: aminoguanidine (AG), a specific inducible nitric oxide synthase (iNOS) inhibitor and NG-nitro-l-arginine methyl ester (L-NAME), a nonselective blocker of NOS isoforms. METHODS: Endothelial (eNOS) and iNOS gene expression was analyzed by reverse transcriptase-polymerase chain reaction. Cirrhotic rats received a single intragastric dose of CCl(4) to induce acute liver damage (ALD). RESULTS: After ALD, aspartate aminotransferase highest levels were observed in rats treated with AG and ALT in rats treated with L-NAME. Inhibitors decreased creatinine serum levels to normal values and serum sodium levels re-established after the third day of ALD. L-NAME diminished (P<0.05) eNOS RNA renal expression. Renal iNOS with no inhibitor was overexpressed but was down-regulated by AG treatment. Liver eNOS RNA expression had a decreased expression before ALD in cirrhotic rats, but L-NAME treatment down-regulated eNOS after ALD. AG induced an important iNOS liver decrease. CONCLUSION: Both inhibitors improved renal function, although AG displayed a better effect and did not aggravate liver function. We concluded that NOS isoforms are implicated in the renal pathophysiologic events induced by ALD. SN - 1478-3223 UR - https://www.unboundmedicine.com/medline/citation/15698410/Nitric_oxide_synthases_inhibition_results_in_renal_failure_improvement_in_cirrhotic_rats_ L2 - https://doi.org/10.1111/j.1478-3231.2005.01018.x DB - PRIME DP - Unbound Medicine ER -