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

D. W. Lipke, S. Oparil, Kenneth Olson

Research output: Contribution to journalArticle

13 Citations (Scopus)

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
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number2 27-2
StatePublished - 1990

Fingerprint

Kinins
Trout
Bradykinin
Blood Vessels
Kallidin
Adrenergic Agents
Plasma Kallikrein
Kallikrein-Kinin System
Intra-Arterial Injections
Tissue Kallikreins
Endothelium-Dependent Relaxing Factors
Captopril
Peptidyl-Dipeptidase A
Prostaglandin-Endoperoxide Synthases
Prostaglandins
Hydrolysis
Lung
Injections

Keywords

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

ASJC Scopus subject areas

  • Physiology

Cite this

@article{81cbb11e89634c4bbaa6652d8f9bd567,
title = "Vascular effects of kinins in trout and bradykinin metabolism by perfused gill",
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.",
keywords = "angiotensin-converting enzyme, blood pressure, bradykinin, fish, kallikrein-kinin system",
author = "Lipke, {D. W.} and S. Oparil and Kenneth Olson",
year = "1990",
language = "English",
volume = "258",
journal = "American Journal of Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "2 27-2",

}

TY - JOUR

T1 - Vascular effects of kinins in trout and bradykinin metabolism by perfused gill

AU - Lipke, D. W.

AU - Oparil, S.

AU - Olson, Kenneth

PY - 1990

Y1 - 1990

N2 - 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.

AB - 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.

KW - angiotensin-converting enzyme

KW - blood pressure

KW - bradykinin

KW - fish

KW - kallikrein-kinin system

UR - http://www.scopus.com/inward/record.url?scp=0025306305&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025306305&partnerID=8YFLogxK

M3 - Article

C2 - 2178453

AN - SCOPUS:0025306305

VL - 258

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0193-1857

IS - 2 27-2

ER -