Vascular effects of kinins in trout and bradykinin metabolism by perfused gill

D. W. Lipke, S. Oparil, K. R. Olson

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

In the preceding studies we have shown that elements of a kallikrein-kinin system (KKS) are present in trout. The present study examines the cardiovascular effects of intra-arterial kinin injection and the ability of perfused gills or gill homogenates to metabolize bradykinin or the pressor substance generated in trout plasma by glandular kallikrein (T60K). Bradykinin (BK), t-kinin, kallidin, and Met-kallidin produced pressor responses in vivo. BK responses were unaffected by α-adrenergic blockade or cyclooxygenase inhibition. Perfused gills extracted ~40% of a [3H]BK bolus, however, metabolites were not recovered from the effluent perfusate. Gill homogenates completely metabolized [3H]BK and inactivated the pressor substance T60K. Captopril reduced BK and T60K metabolism by gill homogenates. The present study demonstrates that kinins have pressor effects in trout that are not mediated through adrenergic or prostanoid-derived mechanisms. The results also suggest that trout do not release endothelium-derived relaxing factors in response to kinin injection. The gill is able to metabolize BK and T60K, although, with respect to BK, this process appears to involve intracellular hydrolysis and may be only partially dependent on angiotensin-converting enzyme. Inactivation of BK by gill tissue may be fundamentally different from kinin metabolism by the mammalian lung.

Original languageEnglish (US)
Pages (from-to)R515-R522
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number2 27-2
DOIs
StatePublished - 1990

Keywords

  • angiotensin-converting enzyme
  • blood pressure
  • bradykinin
  • fish
  • kallikrein-kinin system

ASJC Scopus subject areas

  • Physiology

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