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

Jonsdottir, Ingibjörg H, 1966 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
Johansson, C (författare)
Asea, Alexzander, 1960 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi,Institute of Laboratory Medicine, Dept of Clinical Virology
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Johansson, P (författare)
Hellstrand, Kristoffer, 1956 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi,Institute of Laboratory Medicine, Dept of Clinical Virology
Thorén, Peter (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
Hoffmann, P (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
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 (creator_code:org_t)
1997
1997
Engelska.
Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 160:4, s. 333-9
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

Nyckelord

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

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