Cardiovascular effects of homologous bradykinin in rainbow
trout.
Olson, Kenneth R., Daniel J. Conklin, Leroy Weaver, Jr., Douglas W.
Duff, Ceil A. Herman, Xinying Wang, and J. Michael Conlon.
Indiana University School of Medicine, South Bend Center for
Medical Education, University of Notre Dame, Notre Dame, IN 46556,
Department of Biology, Indiana University, South Bend, South Bend, IN
46634, Department of Biology, New Mexico State University, Las
Cruces, NM 88003, Regulatory Peptide Center, Department of Biomedical
Sciences, Creighton University Medical School, Omaha, NB 68178
APStracts 3:0326R, 1996.
Bradykinins have only recently been identified in fish and a detailed
analysis of their cardiovascular actions is lacking. The present
study examines the cardiovascular effects of trout bradykinin ([Arg0,
Trp5, Leu8]bradykinin; tBK) in conscious trout, Oncorhynchus mykiss.
tBK (1-10 nmol x kg-1 body weight bolus) produced triphasic pressor
-depressor-pressor responses. In phase 1, cardiac output (CO), ventral
and dorsal aortic and central venous pressure (PVA, PDA, PVEN,
respectively) increased, while systemic and gill resistance (RS, Rg)
were unchanged. In phase 2, RG increased, while RS, CO and heart rate
(HR) decreased, reducing PVA and PDA. Plasma prostaglandin E2 (PGE2)
and the prostacyclin metabolite, 6-ketoprostaglandin F1[alpha] (6
-keto PGF1[alpha]), were significantly elevated during phase 2,
whereas, leukotrienes C4 (LTC4), and B4 (LTB4) and thromboxane B2
(TXB2) were unaffected. Phase 3 was produced by an increased CO and
RS and the return of RG to control. Phase 1 pressor response was not
blocked by inhibitors of cyclooxygenase, angiotensin converting
enzyme (ACE), or [alpha]-adrenoceptors ([alpha]-AD), whereas phase 2
depressor and plasma prostaglandin responses were prevented by
cyclooxygenase inhibition. Phase 3 was partially blocked by ACE and
[alpha]-AD inhibitors and is a response to the preceding hypotension.
In vitro, tBK only decreased vascular resistance in the perfused
splanchnic or skeletal muscle-kidney preparations. These results show
that while tBK has multiple effects on the trout cardiovascular
system, none of the effects are due to direct tBK stimulation of
vascular smooth muscle. Phase 2 vasodilation has features consistent
with release of vasodilator prostaglandins while the mechanism of
phase 1 constriction is unknown.
Received 16 February 1996; accepted in final form 23 August 1996.
APS Manuscript Number R98-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996