CARDIOVASCULAR EFFECTS OF HOMOLOGOUS BRADYKININ IN RAINBOW-TROUT

Bradykinins have only recently been identified in fish, and a detailed analysis of their cardiovascular actions is lacking. The present stud y examines the cardiovascular effects of trout bradykinin ([Arg(0),Trp (5),Leu(8)]bradykinin; tBK) in conscious trout, Oncorhynchus mykiss. t BK (1-10 nmol/kg body wt bolus) produced triphasic pressor-depressor-p ressor responses. In phase 1, cardiac output (CO), ventral aortic (P-V A), dorsal aortic (P-DA), and central venous pressure increased, where as systemic (R(S)) and gill resistance (R(G)) were unchanged. In phase 2, R(G) increased, whereas R(S), CO, and heart rate decreased, reduci ng P-VA and PDA Plasma prostaglandin E(2) and the prostacyclin metabol ite, 6-ketoprostaglandin F-1 alpha, were significantly elevated during phase 2, whereas leukotrienes C-4 and B-4 and thromboxane B-2 were un affected. Phase 3 was produced by an increased CO and R(S) and the ret urn of R(G) to control. Phase 1 presser response was not blocked by in hibitors of cyclooxygenase, angiotensin-converting enzyme (ACE) or alp ha-adrenoceptors (alpha-AD), whereas phase 2 depressor and plasma pros taglandin responses were prevented by cyclooxygenase inhibition. Phase 3 was partially blocked by ACE and (alpha-AD inhibitors and is a resp onse to the preceding hypotension. In vitro, tBK only decreased vascul ar resistance in the perfused splanchnic or skeletal muscle-kidney pre parations. These results show that although tBK has multiple effects o n the trout cardiovascular system, none of the effects are due to dire ct 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.