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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 15-20 
    ISSN: 1432-1912
    Keywords: Diazoxide ; Propranolol ; Tachycardia ; Hypotension ; Hyperglycaemia ; Sympathetic reflex activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In unanaesthetized rabbits, diazoxide was injected i.v. in doses of 6.25, 12.5, and 25.0 mg/kg. A dose-dependent fall in blood pressure occurred, while heart rate rose to nearly maximum levels already with the lowest dose. After the medium and the high dose, blood glucose concentration increased continuously within the observation period of 2 h, and plasma concentration of angiotensin II was about 10-fold normal after the same time. Propranolol in doses of 0.67, 2.0, and 6.0 mg/kg, given i.v. 15 min before diazoxide (12.5 mg/kg), had no effect on the hypotensive action of the latter, but inhibited the increase both in heart rate and in blood pressure. The initial rise in heart rate was partly inhibited by 2 mg/kg propranolol, but no further inhibition was obtained by the dose of 6 mg/kg. Blood glucose increase was abolished by 2 mg/kg and markedly suppressed by 6 mg/kg propranolol. Beta-adrenoceptor blockade also reduced the elevated plasma concentration of angiotensin II. It is concluded that the rise in heart rate induced by diazoxide is caused not only by sympathetic stimulation, but also by a direct action on the heart. Similarly, the increase in plasma angiotensin II concentration is in part induced by beta-adrenoceptor stimulation and in addition by a direct renal mechanism. On the other hand, the hyperglycaemic effect seems to depend predominantly upon the stimulation of beta-adrenoceptors.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 43-45 
    ISSN: 1432-1440
    Keywords: Gehirnrenin ; Angiotensin ; Angiotensinogen ; Liquor cerebrospinalis ; Blutdruck ; Brain renin ; Angiotensin ; Angiotensinogen ; Cerebrospinal fluid ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Cerebrospinal fluid (CSF) of rats contains high angiotensinogen concentrations. When 3500-fold purified renin from human brain was injected into the brain ventricles of rats, angiotensin I concentrations increased from undetectable levels to 147.9±18.8 fMol per ml CSF. In parallel, mean arterial blood pressure increased from 93±2.4 mm Hg to 107±3.7 mm Hg. The increase in blood pressure could be abolished by intraventricular administration of saralasin, a blocker of angiotensin II receptors. Intraventricular injection of cathepsin D had no effect on arterial blood pressure and the angiotensin I concentration in CSF remained below detection limits of the radioimmunoassay. We conclude that brain renin acts on endogenous brain angiotensinogen under physiological in vivo conditions to form angiotensin I. The latter is converted to angiotensin II and leads to biological effects, i.e. increase of blood pressure.
    Notes: Zusammenfassung Der Liquor cerebrospinalis von Ratten enthält Angiotensinogen in hoher Konzentration. Nach Injektion von 3500fach angereichertem menschlichem Gehirnrenin in die Hirnventrikel von Ratten stieg die Konzentration von Angiotensin I von unmeßbar niedrigen Werten auf 147,9±18,8 fMol pro ml Liquor an. Der mittlere arterielle Blutdruck änderte sich dabei von 93±2,4 mm Hg auf 107±3,7 mmHg. Der Blutdruckanstieg konnte durch intraventrikuläre Gabe des Angiotensin II Rezeptorenblockers Saralasin rückgängig gemacht werden. Die intraventrikuläre Injektion von Cathepsin D hatte keinen Effekt auf den arteriellen Blutdruck, und die Angiotensin I Konzentration im Liquor blieb unterhalb des Meßbereiches des Radioimmunoassays. Wir schließen daraus, daß Gehirnrenin unter physiologischen Bedingungen in vivo Angiotensin I von endogenem Gehirnangiotensinogen abspaltet. Angiotensin I wird zu Angiotensin II umgewandelt und führt zum Blutdruckanstieg.
    Type of Medium: Electronic Resource
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