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Kinins pp 197-200 | Cite as

Adrenergic and Cholinergic Control of the Activation of the Kallikrein-Kinin System in the Rat Blood

  • A. M. Rothschild
  • J. C. Gomes
  • A. Castania
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 70)

Abstract

Sympathomimetic amines activate the kallikrein system of rat blood, causing up to 50% lowering of kininogen, transient kinin release and transient benzoyl arginine ethyl ester (BAEE) hydrolase activity. The action of catecholamines mimics and could be a model for the study of kallikrein activation and kinin release observed following nerve stimulation (Hilton & Lewis [1], Gautvik, Kriz, Lund-Learsen and Waaler [2], Inoki, Toyoda & Yamamoto [3], Turker & Turker [4], Inoki, Hayashi, Kudo, Matsumoto & Yamamoto [5]). Catecholamine activation of the kininogen-consuming process has the following characteristics:
  1. a)

    reproducible in vitro in rat whole oxaleted blood (6);

     
  2. b)

    not obtained in cell-free plasma nor in plasma containing either platelets, eosinophils, lymphocytes or erythrocytes (7);

     
  3. c)

    effectiveness: epinephrine > nor-epinephrine; isoprenaline ineffective, does not block the action of epinephrine (6);

     
  4. d)

    inhibited by either alpha or beta-adrenergic antagonists, the former being more potent (6);

     
  5. e)

    inhibited by acetylsalicylic acid (Aspirin), bovine kallikrein inhibitor (Trasylol) or soy bean trypsin inhibitor (SBTI) (6,7).

     
  6. f)

    reproducible in rat plasma treated with rat peritoneal fluid cell (PFC) suspensions exposed to epinephrine for 2 min.; not obtained with untreated PFC; after activation by epinephrine, PFC can be centrifuged and washed without loss of their acquired activity (8);

     
  7. g)

    not obtained when PFC free of mast cells are added to plasma in the presence of epinephrine (8);

     
  8. h)

    inhibited by dibutyril cyclic-AMP, 5 × 10−5M (9);

     
  9. i)

    possibly associated with mast cell vacuolization and intracellular granule retraction, a phenomenon observed in epinephrine or nor-epinephrine-treated rat mesentery mast cells (10) which is inhibited by Aspirin (8), at the same concentrations which block kininogen depletion;

     
  10. j)

    epinephrine activation of kallikrein in the presence of PFC is not accompanied by the release of histamine from such cells. Increased amounts of histamine are however observed in the tissues of epinephrine-treated rats (11, 12); they are to be attributed to enhanced, short-term synthesis of histamine induced by epinephrine, (Rosengren & Svensson) (13);

     
  11. k)

    kininogen depletion and mast cell vacuolization apparently identical to those produced by catecholamines, are shown in rats treated with carbamylcholine, a cholinergic agonist. The effect on kininogen can also be shown in vitro, in oxalated blood incubated for 5 min. with carbamylcholine. This excludes reflexly released catecholamines as mediators of kallikrein activation in carbamylcholine treated rats.

     

Keywords

Mast Cell Cholinergic Agonist Sympathomimetic Amine Kallikrein Activation Catecholamine Activation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

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  2. 2.
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Copyright information

© Plenum Press, New York 1976

Authors and Affiliations

  • A. M. Rothschild
    • 1
  • J. C. Gomes
    • 1
  • A. Castania
    • 1
  1. 1.Department of Pharmacology, School of Medicine of Ribeirao PretoUSPBrazil

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