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/kg body wt bolus) produced triphasic pressor-depressor- pressor responses. In phase 1, cardiac output (CO), ventral aortic (P(VA)), dorsal aortic (P(DA)), and central venous pressure increased, whereas systemic (R(s)) and gill resistance (R(G)) were unchanged. In phase 2, R(G) increased, whereas R(s), CO, and heart rate decreased, reducing P(VA) and P(DA). Plasma prostaglandin E2 and the prostacyclin metabolite, 6- ketoprostaglandin F(1α), were significantly elevated during phase 2, whereas leukotrienes C1 and B4 and thromboxane B2 were unaffected. Phase 3 was produced by an increased CO and R(S) and the return of R(G) to control. Phase 1 presser response was not blocked by inhibitors of cyclooxygenase, angiotensin-converting enzyme (ACE) or α-adrenoceptors (α-AD), whereas phase 2 depressor and plasma prostaglandin responses were prevented by cyclooxygenase inhibition. Phase 3 was partially blocked by ACE and α-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 although 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.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||4 41-4|
|Publication status||Published - 1997|
- endothelium-derived relaxing factor
- kallikrein-kinin system
ASJC Scopus subject areas
- Physiology (medical)