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      Antonín Vančura and Arterial Hypertension

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          A historical overview of the important contributions of Prof. Antonin Vančura from Charles University Medical Faculty, Prague, to the broader understanding of the pathogenesis, clinical course and classification of arterial hypertension is given in his pivotal publication and first Czech monography ‘High Blood Pressure’. His unique clinical series of 1,096 hypertensive patients with their long-term follow-up after 5, 10 and 15 years made it possible to work out the classification of hypertension not only on the basis of blood pressure readings, but also according to target organ damage – a principle which is close to the 2003 classification of the European Society of Hypertension/European Society of Cardiology (ESH/ESC). In agreement with today’s conception, Vančura emphasized already in 1942 the importance of metabolic changes and albuminuria for prognosis of the disease. In spite of the technical, instrumental and laboratory limitations, it is possible to gain from Vančura’s publication a modern interpretation of his results given by a long-term follow-up of this large group of patients. In many ways, Vančura outstripped his time and his concepts approached today’s standings and so founded one of the important schools of hypertension in Czechoslovakia and Europe.

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          Hypertension and associated metabolic abnormalities--the role of insulin resistance and the sympathoadrenal system.

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            1. Renin reacts with renin-activator to form a strong pressor substance which is heat-stable, water- and alcohol-soluble, fluorescent, acid-stable, and alkali-labile. It is a reducing substance and is destroyed by strong oxidizing substances. It forms crystalline salts with oxalic and picric acids. The color reaction for arginine is the only one found to be strongly positive. It is suggested that this substance be called angiotonin. 2. Angiotonin produces a sharp, immediate rise in arterial pressure when injected intravenously. Pithing and dissipation of the anesthetic appear to increase the response. Tachyphylaxis occurs, in contrast to renin, only after many single doses. 3. The responses to adrenaline and angiotonin do not parallel one another. Cocaine, atropine, and stilbestrol do not affect the pressor action of angiotonin. Suprarenalectomy in brief experiments is also without effect. 4. Maximal amounts of angiotonin result when the proportion between renin and activator is roughly 3 to 100. This is not a stoichiometric relationship in the chemical sense. The temperature suitable for good yields is about 38°C., and the time of reaction from 10 to 20 minutes. 5. Renin destroys angiotonin when incubated with it. 6. Angiotonin causes marked contraction of intestinal segments of rabbits without reducing their rhythmic motion. It sensitizes the intestine to further doses of angiotonin and alters the intestine such that renin-activator contracts it. Angiotonin also constricts the vessels of a rabbit's ear perfused with blood or Ringer's solution.

              Author and article information

              Kidney Blood Press Res
              Kidney and Blood Pressure Research
              S. Karger AG
              November 2006
              17 November 2006
              : 29
              : 4
              : 237-242
              2nd Department of Medicine, Charles University 1st School of Medicine and University General Hospital, Prague, Czech Republic
              95913 Kidney Blood Press Res 2006;29:237–242
              © 2006 S. Karger AG, Basel

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              Figures: 2, Tables: 5, References: 12, Pages: 6
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