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Research ArticleArticle

The Effects of Stress on Homeostasis in JCR-LA-cp Rats: The Role of Nitric Oxide

Juan C. Leza, Eduardo Salas, Grzegorz Sawicki, James C. Russell and Marek W. Radomski
Journal of Pharmacology and Experimental Therapeutics September 1998, 286 (3) 1397-1403;
Juan C. Leza
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Eduardo Salas
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Grzegorz Sawicki
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James C. Russell
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Marek W. Radomski
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Abstract

We have investigated the effects of early phases of chronic stress on generation and actions of nitric oxide (NO) in JCR:LA-cp rats both lean (+/+) and obese (cp/cp). Restraint stress was carried out for a 15-min single exposure or for 1 hr every day during 4, 9 or 14 days. The stress reaction was evidenced by significant increase in plasma cortisol. The exposure to stress for 14 days led to a neuronal damage in lean rats as evidenced by a decrease in glutamate uptake and an increase in the release of lactate in synaptosomes. This effect was not observed in obese rats. Concomitantly, the levels of glutamate increased in the hippocampus at 14 days in lean, but not obese rats, that showed higher basal levels of glutamate than lean rats. The activity of NO synthase (NOS) and guanosine cyclic monophosphate levels increased in the hippocampus preceding the neuronal damage. The neuronal lesions were prevented by inhibition of NOS without affecting cortisol levels. In the cardiovascular system, chronic stress exerted no significant effect on blood pressure, aortic contractility or platelet aggregation. However, there were significant changes in plasma nitrite/nitrate that reached maximum at 4 to 9 days. It is concluded that the generation of NO contributes to the systemic response to the organism to stress. In the brain, NO appears to be detrimental as this molecule mediates glutamate-dependent hippocampal damage, this effect being cortisol-independent. In contrast, in the vascular system, increased generation of NO may attenuate the vasoconstrictor and platelet aggregatory effects of catecholamines and other mediators of stress.

Footnotes

  • Send reprint requests to: Dr. Juan C Leza, Department of Pharmacology, Universidad Complutense, Madrid 28040, Spain.

  • ↵1 This work was supported by UCM 97/7154 and DGICYT PR 97/0054 Spain to J.C.L. J.C.L. is a recipient of a grant from the Spanish Ministry of Education and Science (PR 95/435), E.S. is an Alberta Heritage Foundation for Medical Research (AHFMR)-Eli Lilly post-doctoral fellow and M.W.R. is an AHFMR scholar.

  • Abbreviations:
    NO
    nitric oxide
    NOS
    nitric oxide synthase
    cGMP
    guanosine 3′-5′-cyclic monophosphate
    L-NAME
    NG-nitro-l-arginine methyl ester
    EAA
    excitatory amino acid
    CNS
    central nervous system
    LDH
    lactate dehydrogenase
    eNOS
    endothelial NOS
    nNOS
    neuronal NOS
    iNOS
    inducible NOS
    L-NAME
    NG-nitro-l-arginine methyl ester
    HPLC
    high-performance liquid chromatography
    • Received February 12, 1998.
    • Accepted April 29, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 286, Issue 3
1 Sep 1998
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Research ArticleArticle

The Effects of Stress on Homeostasis in JCR-LA-cp Rats: The Role of Nitric Oxide

Juan C. Leza, Eduardo Salas, Grzegorz Sawicki, James C. Russell and Marek W. Radomski
Journal of Pharmacology and Experimental Therapeutics September 1, 1998, 286 (3) 1397-1403;

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Research ArticleArticle

The Effects of Stress on Homeostasis in JCR-LA-cp Rats: The Role of Nitric Oxide

Juan C. Leza, Eduardo Salas, Grzegorz Sawicki, James C. Russell and Marek W. Radomski
Journal of Pharmacology and Experimental Therapeutics September 1, 1998, 286 (3) 1397-1403;
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