Plasma kinins and cortisol: a possible explanation of the anti-inflammatory action of cortisol.
Kinins are naturally occurring vasoactive polypeptides thought to be mediators of acute inflammatory responses. Kinins are released from a plasma protein substrate by glass-activated plasma enzymes (kallikreins) or by isolated intact granulocytes. Cortisol in concentrations of 2.5 x 10(-6) to 2.5 x 10(-5)M prevented the release of active kinin from substrate by granulocytes or contact with glass. Deoxycorticosterone, progesterone, and etiocholanolone in comparable concentrations were significantly less effective in preventing kinin release. Plasma obtained from patients receiving prednisone released no kinin after activation by glass and less kinin than control plasma when exposed to granulocytes. Cortisol also partially inhibited the release of kinin by purified urinary kallikrein. Certain adrenocorticosteroids may exert their anti-inflammatory effect by inhibiting the release of plasma kinins. Steroids may act in part by preventing interaction between the activated kallikrein and its substrate.
D000818:Animals; D001681:Biological Assay; D003900:Desoxycorticosterone / Q000494:pharmacology*; D005043:Etiocholanolone / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007610:Kallikreins / Q000494:pharmacology*; D007705:Kinins / Q000378:metabolism*; D007962:Leukocytes / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology*; D051381:Rats; D014599:Uterus / Q000187:drug effects
D007705:Kinins; D003900:Desoxycorticosterone; D011374:Progesterone; D005043:Etiocholanolone; D007610:Kallikreins; D006854:Hydrocortisone