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  • 1975-1979  (2)
  • Hyperglycaemia  (1)
  • Receptors  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Saralasin ; Angiotensin II ; Renin ; Rezeptoren ; Blutdruck ; Saralasin ; Angiotensin II ; Renin ; Receptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 µg/kg × min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 µg/kg × min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 µg/kg × min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypoor hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.
    Notes: Zusammenfassung Ein verbesserter Test zur Diagnose Renin-abhängiger Bluthochdruckformen mit dem Angiotensin II Rezeptor Antagonisten Saralasin wurde in hypertensiven Ratten, sowie in normotensiven und hypertensiven Patienten geprüft. Kumulative intravenöse Dosen, beginnend mit 0,01 µg/kg × min Saralasin wurde alle 15 Minuten um das zehnfache gesteigert. Ein signifikanter Blutdruckabfall bei der Dosis von 0,1 µg/kg × min wurde bei Ratten mit renaler Hypertonie, bei Patienten mit renaler Hypertonie und bei Patienten nach Diuretika-Vorbehandlung gefunden. Plasmaspiegel von Angiotensin I, Angiotensin II, Plasma Renin Aktivität und Saralasin wurden gemessen. Bei der niedrigsten Infusionsrate von 0,01 µg/kg × min waren die Saralasin-Konzentrationen im Plasma 40fach höher als die Plasma Angiotensin II-Konzentrationen. Der Blutdruckabfall erfolgte bei niedrigeren Dosen von Saralasin als der Anstieg von Plasma-Renin als Folge einer Hemmung des feedbacks der Reninsekretion. Die Ergebnisse zeigen, daß Komplikationen wie schwerwiegende Blutdruckanstiege und -abfälle bei schrittweiser Erhöhung der Saralasin-Infusionsrate vermieden werden können; gleichzeitig wird die diagnostische Zuverlässigkeit des Tests erhöht. Der geringe Angiotensin-ähnliche, blutdrucksteigernde Effekt von Saralasin bei Patienten mit niedrigem Renin wird als Vorteil ausgenutzt und erhöht den Unterschied der Blutdruckantwort bei Patienten mit hohem Plasma-Renin und Blutdruckabfall nach Saralasin-Infusion.
    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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