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THE SITE OF ANGIOTONIN DESTRUCTION
1. Theoretical considerations render it unlikely that the greatest part of the angiotonase found in the organism is available for the destruction of angiotonia. A priori considerations support the view that only plasma angiotonase is involved in angiotonin destruction in vivo. 2. We have utilized th...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1946
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135598/ https://www.ncbi.nlm.nih.gov/pubmed/19871540 |
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author | Sapirstein, Leo A. Reed, Racheal K. Page, Ernest W. |
author_facet | Sapirstein, Leo A. Reed, Racheal K. Page, Ernest W. |
author_sort | Sapirstein, Leo A. |
collection | PubMed |
description | 1. Theoretical considerations render it unlikely that the greatest part of the angiotonase found in the organism is available for the destruction of angiotonia. A priori considerations support the view that only plasma angiotonase is involved in angiotonin destruction in vivo. 2. We have utilized the magnitude and duration of the presser response to angiotonin as an index of available angiotonase, and we have found that: (a) Nephrectomy and evisceration are without marked effect on angiotonin response. (b) Hemorrhage and hemodilution without shock cause a striking increase in the response to angiotonin and this appears to be due to removal of the plasma rather than the cells. Shock developing after hemorrhage results in a state of refractoriness to angiotonin. (c) Intact red cells in vitro have no destructive action on angiotonin, but after hemolysis they have several hundred times the activity of plasma, (d) Intravascular hemolysis, whether produced in vitro or in vivo, decreases the response to angiotonin to a degree which is consistent with the hypothesis that the normal animal destroys angiotonin entirely in its plasma. The active principle in hemolyzed blood is destroyed by heating to 65–70°C. for 15 minutes. 3. These findings support the hypothesis that all or at least the greatest part of angiotonin destruction under physiological circumstances occurs in the plasma, and the significance of this hypothesis is discussed. |
format | Text |
id | pubmed-2135598 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1946 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21355982008-04-18 THE SITE OF ANGIOTONIN DESTRUCTION Sapirstein, Leo A. Reed, Racheal K. Page, Ernest W. J Exp Med Article 1. Theoretical considerations render it unlikely that the greatest part of the angiotonase found in the organism is available for the destruction of angiotonia. A priori considerations support the view that only plasma angiotonase is involved in angiotonin destruction in vivo. 2. We have utilized the magnitude and duration of the presser response to angiotonin as an index of available angiotonase, and we have found that: (a) Nephrectomy and evisceration are without marked effect on angiotonin response. (b) Hemorrhage and hemodilution without shock cause a striking increase in the response to angiotonin and this appears to be due to removal of the plasma rather than the cells. Shock developing after hemorrhage results in a state of refractoriness to angiotonin. (c) Intact red cells in vitro have no destructive action on angiotonin, but after hemolysis they have several hundred times the activity of plasma, (d) Intravascular hemolysis, whether produced in vitro or in vivo, decreases the response to angiotonin to a degree which is consistent with the hypothesis that the normal animal destroys angiotonin entirely in its plasma. The active principle in hemolyzed blood is destroyed by heating to 65–70°C. for 15 minutes. 3. These findings support the hypothesis that all or at least the greatest part of angiotonin destruction under physiological circumstances occurs in the plasma, and the significance of this hypothesis is discussed. The Rockefeller University Press 1946-04-30 /pmc/articles/PMC2135598/ /pubmed/19871540 Text en Copyright © Copyright, 1946, by The Rockefeller Institute for Medical Research New York This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Sapirstein, Leo A. Reed, Racheal K. Page, Ernest W. THE SITE OF ANGIOTONIN DESTRUCTION |
title | THE SITE OF ANGIOTONIN DESTRUCTION |
title_full | THE SITE OF ANGIOTONIN DESTRUCTION |
title_fullStr | THE SITE OF ANGIOTONIN DESTRUCTION |
title_full_unstemmed | THE SITE OF ANGIOTONIN DESTRUCTION |
title_short | THE SITE OF ANGIOTONIN DESTRUCTION |
title_sort | site of angiotonin destruction |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135598/ https://www.ncbi.nlm.nih.gov/pubmed/19871540 |
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