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Duration and mechanisms of the increased natural cytotoxicity seen after chronic voluntary exercise in rats.

Artikel i vetenskaplig tidskrift
Författare Ingibjörg H Jonsdottir
C Johansson
Alexzander Asea
P Johansson
Kristoffer Hellstrand
Peter Thorén
P Hoffmann
Publicerad i Acta physiologica Scandinavica
Volym 160
Nummer/häfte 4
Sidor 333-9
ISSN 0001-6772
Publiceringsår 1997
Publicerad vid Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi
Sidor 333-9
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adrenergic beta-Antagonists, pharmacology, Animals, Catecholamines, physiology, Cell Survival, physiology, Exertion, physiology, Histamine, physiology, Histamine H2 Antagonists, pharmacology, Naloxone, pharmacology, Narcotic Antagonists, pharmacology, Ranitidine, pharmacology, Rats, Rats, Inbred SHR, Timolol, pharmacology, Tumor Cells, Cultured
Ämneskategorier Fysiologi

Sammanfattning

We have recently shown that in vivo natural cytotoxicity is enhanced after chronic exercise in spontaneously hypertensive rats (SHRs). In the present report, we have studied the duration of this augmentation and some possible mechanisms involved. Exercise consisted of voluntary running for 4-5 weeks, with the running distance ranging from 2.7-15.6 km day(-1) during the last week of running. In vivo cytotoxicity was measured as clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs. The in vivo natural cytotoxicity was increased in running SHRs, and also in SHRs that had their running wheel locked for 24 and 48 h prior to the experiment, and was still present after 96 h. The enhancement of in vivo cytotoxicity after 5 weeks of exercise was abolished after an acute injection of the beta-adrenergic receptor antagonist timolol (0.5 mg kg(-1) i.v.), indicating that catecholamines are involved in this augmentation. Interestingly, 24 h after the last exercise bout, the increased natural cytotoxicity could be blocked by timolol. The opioid receptor antagonist naloxone given subcutaneously for 7 days by osmotic pumps (6 mg kg(-1) h(-1)) could not reverse the increased in vivo cytotoxicity seen in the running SHRs, suggesting that opioid receptor mechanisms are not involved, or at least not the naloxone-sensitive mu-receptor. Natural immunity was not influenced by the histamine H2 receptor antagonist ranitidine, either in controls or in runners, indicating that the natural killer cell-regulatory effect of histamine is not present in SHRs and does not seem to be involved in the exercise-induced changes in natural immune function. We conclude that the augmentation of in vivo natural cytotoxicity after voluntary chronic exercise in rats is long-lasting and that the augmentation is partly mediated by beta-adrenergic receptors.

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