title: Evidence that cortisol may protect against the immediate effects of stress on circulating leukocytes in the trout.
abstract: Rainbow trout stressed by an intraperitonal injection of saline displayed reduced phagocytic activity of their spleen and head-kidney macrophages within 3 hr. Phagocytic activity was similarly depressed by injecting noradrenalin, but was maintained in fish injected with the adrenergic blocking agent phentolamine, suggesting that endogenous catecholamines are involved in this stress response. Since stress may increase the number of circulating granulocytes, it is proposed that noradrenalin, released during stress, causes the liberation of active macrophages from the lymphocytic tissue, the remaining macrophages therefore showing a lowered phagocytic index. Cortisol injection, like phentolamine, prevented the depressive effect of stress on the phagocytic index but did not antagonize the depressive effect of exogenous noradrenalin. It is suggested that the stress-induced release of endogenous catecholamines may be prevented by cortisol. Injection stress caused a decline in the number of circulating lymphocytes/thrombocytes, indicating their retrafficking into some other tissue. This was opposed by cortisol and by high doses of noradrenalin. It is proposed that cortisol or noradrenalin may oppose, directly or indirectly, the expression of adhesion molecules which are normally induced after stress.
authors.affiliation: School of Biology and Biochemistry, Bath University, Bath, BA2 7AY, United Kingdom.
authors.forename: Y K
authors.initials: YK
authors.lastname: Narnaware
authors.forename: B I
authors.initials: BI
authors.lastname: Baker
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D006854:Hydrocortisone / Q000097:blood / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D018655:Lymphocyte Count / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D017686:Oncorhynchus mykiss; D009929:Organ Size; D010587:Phagocytosis / Q000187:drug effects* / Q000502:physiology; D010646:Phentolamine / Q000494:pharmacology; D011863:Radioimmunoassay; D012965:Sodium Chloride / Q000494:pharmacology; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D013312:Stress, Physiological / Q000276:immunology / Q000503:physiopathology*; D013565:Sympatholytics / Q000494:pharmacology; D013566:Sympathomimetics / Q000494:pharmacology; D013696:Temperature
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D013565:Sympatholytics; D013566:Sympathomimetics; D012965:Sodium Chloride; D006854:Hydrocortisone; D009638:Norepinephrine; D010646:Phentolamine