AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 2 501-R506, Copyright © 1990 by American Physiological Society
Enzymes of the kallikrein-kinin system in rainbow trout
D. W. Lipke and K. R. Olson
Department of Biological Sciences, University of Notre Dame, Indiana 46556.
Evidence for a kallikrein-kinin system (KKS) in fish is incomplete. In the
present study, components of the KKS were identified in rainbow trout.
Tissues were assayed for kallikrein-like esterolytic activity using three
synthetic kallikrein substrates (TAME, VGAN, and PPAN), and the presence of
kallikrein substrate (kininogen) in trout plasma was estimated by
bradykinin (BK) radioimmunoassay of plasma activated with trypsin (T).
Formation of pressor-depressor substances in vivo by porcine glandular
kallikrein (GK) and T was measured after intra-arterial injection into
unanesthetized trout. Gill and kidney contained kallikrein activity (TAME
and VGAN assays); little activity was observed with PPAN. Aprotinin
inhibited gill activity (TAME assay). T liberated 42 +/- 3 (SE) ng (n = 10)
of immunoreactive BK per milliliter of plasma. Injection of GK in vivo
reduced plasma kininogen levels for over 24 h. GK produced pressor
responses only in fish pretreated with the angiotensin-converting enzyme
(ACE) inhibitor captopril. This effect was mediated partly through
stimulation of alpha-adrenergic receptors. T produced slight pressor
responses that were captopril insensitive. These results show that trout
possess elements of the KKS system including kallikrein-like enzymatic
activity, kininogen, receptor-mediated vascular sensitivity to kallikrein
products, and kininolytic activity consistent with ACE (kininase II).
