In Field-Stimulated Guinea-Pig Atria an AT1-Receptor Mediated Increase of Noradrenaline Release by Angiotensin II is Seen only in the Presence of Prejunctional Autoinhibition

  • H. Brasch
  • L. Sieroslawski
  • N. Bergmann
  • P. Dominiak
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 377)

Abstract

The octapeptide angiotensin II is a potent vasoconstrictor and increases the release of adrenaline from the adrenal medulla and noradrenaline from the terminal reticulum of sympathetic nerves. The main source of angiotensin II in plasma is angiotensinogen, which is metabolized to angiotensin I by renin secreted from the kidneys and then to the active compound angiotensin II by a circulating angiotensin converting enzyme. There is increasing evidence, however, that angiotensin II can also be produced locally in a variety of tissues. In the heart angiotensin I, II and III are present and a messenger RNA for the synthesis of renin as well as a tissue-bound converting enzyme have been detected (Lindpainter et al. 1987). This local renin-angiotensin system seems to be involved in the regulation of cell growth and may be an important factor for the development of cardiac hypertrophy (Linz et al. 1989). It can also participate in the local control of the sympathetic tone by an activation of prejunctional angiotensin receptors on nerve terminals (Ziogas et al. 1984).

Keywords

Refractory Period Electrical Field Pulse Field Pulse Noradrenaline Release Stimulation Period 
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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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • H. Brasch
    • 1
  • L. Sieroslawski
    • 1
  • N. Bergmann
    • 1
  • P. Dominiak
    • 1
  1. 1.Institute of PharmacologyMedical University LübeckLübeckGermany

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