AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 2 507-R514, Copyright © 1990 by American Physiological Society
Generation of vasoactive substances in trout and rat plasma by trypsin and kallikrein
D. W. Lipke, K. D. Meisheri and K. R. Olson
Department of Biological Sciences, University of Notre Dame, Indiana.
In the preceding study we demonstrated kallikrein-like enzymatic activity
in trout tissues and showed that kallikrein incubated with trout plasma
(T60K) produces a vasopressor substance(s). The present study further
examines the effects of T60K in fish and mammals in vitro and in vivo. T60K
produced a dose-dependent pressor response in both trout and rats, whereas
kallikrein-activated rat plasma (R60K) was pressor in trout and depressor
in rats. Captopril did not affect the response of rats to T60K or R60K.
Phenoxybenzamine attenuated the T60K response in trout but not in rats,
thus T60K effects in trout are partially mediated through catecholamines.
Blockade of angiotensin II (ANG II) receptors in rats with [Sar1,Ala8]-ANG
II abolished the pressor effects of T60K. T60K produced dose-dependent
contractions in isolated trout and rabbit arteries; ANG II was ineffective
in trout arteries. T60K-contracted trout arteries were relaxed by atrial
natriuretic peptide and forskolin, whereas diltiazem and sodium
nitroprusside were without effect. [Sar1,Ala8]ANG II inhibited T60K-induced
contractions of rabbit arteries and relaxed rings previously contracted
with T60K. The active component of T60K has a molecular weight less than
10,000, is heat stable, and is inactivated by peptidases. It is
immunologically different than mammalian angiotensins but binds to and
displaces radiolabeled ANG II from ANG II receptors. These results suggest
that kallikrein forms a vasoactive substance(s) in trout plasma that is
neither bradykinin nor ANG II but is similar to the latter in its
pharmacological effects.
