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Increase in neurogenic nitric oxide metabolism by endothelin-1 in mesenteric arteries from hypertensive rats.
J Cardiovasc Pharmacol. 2000 Nov; 36(5):541-7.JC

Abstract

We investigated, in mesenteric arteries from hypertensive rats (SHRs), the possible changes in neurogenic nitric oxide (NO) release produced by endothelin-1 (ET-1), and the mechanisms involved in this process. The contractile response induced by electrical field stimulation (EFS; 200 mA, 0.3 ms, 1-16 Hz, for 30 s) in deendotheliumized mesenteric segments was abolished by tetrodotoxin and phentolamine. The NO synthase inhibitor N(G)-nitro-L-arginine (L-NAME, 10 microM) increased the contractions caused by EFS. ET-1 enhanced the contraction induced by EFS, which was unaltered by the subsequent addition of L-NAME. The ETA antagonist-receptor BQ-123 (1 microM) inhibited the effect of ET-1 on EFS response, whereas the ETB antagonist-receptor BQ-788 (3 microM) partially blocked it, and the subsequent addition of L-NAME restored the contractile response in both cases. SOD (25 unit/ml) decreased the response to EFS, and the subsequent addition of L-NAME increased this response. ET-1 did not modify the decrease in EFS response induced by SOD, and the addition of L-NAME increased the response. None of these drugs altered the response to exogenous noradrenaline (NA) or basal tone except SOD, which increased the basal tone, an effect blocked by phentolamine (1 microM). In arteries preincubated with [3H]NA, ET-1 did not modify the tritium efflux evoked by EFS, which was diminished by SOD. ET-1 did not alter basal tritium efflux, whereas SOD significantly increased the efflux. These results suggest that EFS of SHR mesenteric arteries releases neurogenic NO, the metabolism of which is increased in the presence of ET-1 by the generation of superoxide anions.

Authors+Show Affiliations

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.No 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

11065212

Citation

Ferrer, M, et al. "Increase in Neurogenic Nitric Oxide Metabolism By Endothelin-1 in Mesenteric Arteries From Hypertensive Rats." Journal of Cardiovascular Pharmacology, vol. 36, no. 5, 2000, pp. 541-7.
Ferrer M, Alonso MJ, Salaices M, et al. Increase in neurogenic nitric oxide metabolism by endothelin-1 in mesenteric arteries from hypertensive rats. J Cardiovasc Pharmacol. 2000;36(5):541-7.
Ferrer, M., Alonso, M. J., Salaices, M., Marín, J., & Balfagón, G. (2000). Increase in neurogenic nitric oxide metabolism by endothelin-1 in mesenteric arteries from hypertensive rats. Journal of Cardiovascular Pharmacology, 36(5), 541-7.
Ferrer M, et al. Increase in Neurogenic Nitric Oxide Metabolism By Endothelin-1 in Mesenteric Arteries From Hypertensive Rats. J Cardiovasc Pharmacol. 2000;36(5):541-7. PubMed PMID: 11065212.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increase in neurogenic nitric oxide metabolism by endothelin-1 in mesenteric arteries from hypertensive rats. AU - Ferrer,M, AU - Alonso,M J, AU - Salaices,M, AU - Marín,J, AU - Balfagón,G, PY - 2000/11/7/pubmed PY - 2001/3/3/medline PY - 2000/11/7/entrez SP - 541 EP - 7 JF - Journal of cardiovascular pharmacology JO - J Cardiovasc Pharmacol VL - 36 IS - 5 N2 - We investigated, in mesenteric arteries from hypertensive rats (SHRs), the possible changes in neurogenic nitric oxide (NO) release produced by endothelin-1 (ET-1), and the mechanisms involved in this process. The contractile response induced by electrical field stimulation (EFS; 200 mA, 0.3 ms, 1-16 Hz, for 30 s) in deendotheliumized mesenteric segments was abolished by tetrodotoxin and phentolamine. The NO synthase inhibitor N(G)-nitro-L-arginine (L-NAME, 10 microM) increased the contractions caused by EFS. ET-1 enhanced the contraction induced by EFS, which was unaltered by the subsequent addition of L-NAME. The ETA antagonist-receptor BQ-123 (1 microM) inhibited the effect of ET-1 on EFS response, whereas the ETB antagonist-receptor BQ-788 (3 microM) partially blocked it, and the subsequent addition of L-NAME restored the contractile response in both cases. SOD (25 unit/ml) decreased the response to EFS, and the subsequent addition of L-NAME increased this response. ET-1 did not modify the decrease in EFS response induced by SOD, and the addition of L-NAME increased the response. None of these drugs altered the response to exogenous noradrenaline (NA) or basal tone except SOD, which increased the basal tone, an effect blocked by phentolamine (1 microM). In arteries preincubated with [3H]NA, ET-1 did not modify the tritium efflux evoked by EFS, which was diminished by SOD. ET-1 did not alter basal tritium efflux, whereas SOD significantly increased the efflux. These results suggest that EFS of SHR mesenteric arteries releases neurogenic NO, the metabolism of which is increased in the presence of ET-1 by the generation of superoxide anions. SN - 0160-2446 UR - https://www.unboundmedicine.com/medline/citation/11065212/Increase_in_neurogenic_nitric_oxide_metabolism_by_endothelin_1_in_mesenteric_arteries_from_hypertensive_rats_ L2 - https://doi.org/10.1097/00005344-200011000-00001 DB - PRIME DP - Unbound Medicine ER -