Differences in hormonal and inflammatory parameters in male Lewis and Long Evans rats with adjuvant arthritis.
The purpose of the present study was (i) to compare secretory responses of prolactin and corticosterone to the acute stress of immobilization in male rats of the Lewis and Long Evans strains and (ii) to compare secretion of the two hormones in rats with fully developed adjuvant arthritis (AA) and their relationship with the intensity of the inflammatory reaction. A short immobilization of 5 min induced equal elevations of both hormones in both strains, but 20-min immobilization produced significantly stronger responses in Long Evans rats than in Lewis rats. AA inhibited prolactin secretion equally in both strains (from 11.6 +/- 1.3 ng/ml to 4.2 +/- 0.6 ng/ml in Lewis rats, p < 0.01, and from 3.7 +/- 0.6 to 2.12 +/- 0.1 ng/ml in Long Evans rats, p < 0.05), but caused a conspiciously larger elevation of corticosterone in the Long Evans than in the Lewis animals (11.5 +/- 1.2 microg/dl in Long Evans rats versus 5.1 +/- 0.5 microg/dl in Lewis rats, p < 0.01) while basal levels were similar. The larger corticosterone response in the Long Evans rats was associated with a stronger inflammatory reaction assessed by hind paw swelling (2.3 +/- 0.1 ml for Long Evans rats versus 1.8 +/- 0.08 ml for Lewis rats, p < 0.01) and plasma levels of nitric oxide (47.5 +/- 5.7 microM for Long Evans rats versus 28.7 +/- 2.5 microM for Lewis rats, p < 0.01) than in the Lewis males with lower corticosterone levels. In conclusion, there are significant, obviously genetically based, differences in the corticosterone responses to both immobilization and AA between the two strains, with the Long Evans rats reacting more strongly than the Lewis rats. The lack of the expected inverse relationship between corticosterone levels and the intensity of the inflammation indicates that the activity of corticosterone is not its primary determinant and that other important factors are involved.
Parara
S
S
Department of Normal, Pathological and Clinical Physiology, Third Medical Faculty, Charles University, Prague, Czech Republic.
Seres
J
J
Rokyta
R
R
Stancíková
M
M
Jurcovicová
J
J
D000818:Animals; D001169:Arthritis, Experimental / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D003345:Corticosterone / Q000097:blood / Q000378:metabolism*; D006728:Hormones / Q000097:blood / Q000378:metabolism*; D007249:Inflammation / Q000150:complications* / Q000473:pathology; D008297:Male; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew; D020318:Rats, Long-Evans; D013045:Species Specificity
D006728:Hormones; D011388:Prolactin; D003345:Corticosterone