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  • 1
    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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  • 2
    ISSN: 1432-1440
    Keywords: Blutdruck ; Angiotensin II ; Propranolol ; Spontan hypertensive Ratten ; Gehirn ; Blood pressure ; Angiotensin II ; Propranolol ; Spontaneously hypertensive rats ; Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The blood pressure responses following infusions of angiotensin II (ANG II) into the brain ventricles (i.v.t.) have been tested in spontaneously hypertensive (SH) rats and in normotensive Wistar Kyoto (WK) rats. The mean arterial blood pressure increases were significantly higher in SH rats than in WK rats. Propranolol treatment reduced blood pressure increases to i.v.t. ANG II in WK, but not in SH rats. The higher sensitivity to i.v.t. ANG II in SH rats supports a role of central ANG II in the maintenance of high blood pressure in SH rats.
    Notes: Zusammenfassung Angiotensin II (ANG II) wurde spontan hypertensiven (SH) Ratten und normotensiven Wistar Kyoto (WK) Ratten in den lateralen Hirnventrikel (i.v.t.) infundiert. Der mittlere arterielle Blutdruck stieg bei den SH Ratten signifikant höher an als bei den normotensiven WK Ratten. Propranolol-Vorbehandlung reduzierte die Blutdruckanstiege nach i.v.t. ANG II Infusionen bei WK Ratten, nicht aber bei SH Ratten. Die höhere ANG II Empfindlichkeit der SH Raten bestätigt frühere Ergebnisse, die darauf hinweisen, daß zentrales ANG III an der Aufrechterhaltung des hohen Blutdruckes von SH Ratten beteiligt sein kann.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 31-41 
    ISSN: 1432-1440
    Keywords: Renin ; Angiotensin ; Neurohormone ; Gehirn ; Blutdruck ; Renin ; Angiotensin ; Neurohormones ; Brain ; Blood-Pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Angiotensin circulates in the blood as a hormone. Its main target organs are vascular smooth muscle, adrenal gland and the kidney. Hormonal angiotensin increases blood pressure by its vasoconstrictor action, by stimulation of aldosterone secretion and subsequent sodium and water retention, and by the stimulation of catecholamine release. Circulating plasma angiotensin also effects brain mechanisms of blood pressure regulation. In addition to this hormonal function, angiotensin is present in the brain as part of an endogenous brain renin-angiotensin system. Brain angiotensin is not secreted into the blood and can be considered a neurohormone with local function. A role of brain angiotensin in the maintenance of high blood pressure of spontaneously hypertensive rats has been demonstrated. Circulating plasma angiotensin appears to influence brain renin levels and vice versa. Stimulation of specific areas in the brain known to be involved in the regulation of the cardiovascular system, stimulate renin secretion from the kidney. The renin-angiotensin system can therefore serve as an example for the intimate interrelationship between humoral and neurohumoral mechanisms of blood pressure regulation.
    Notes: Zusammenfassung Angiotensin zirkuliert als Hormon im Blut. Seine wesentlichen Zielorgane sind die glatte Gefäßmuskulatur, die Nebenniere und die Niere. Zirkulierendes hormonales Angiotensin erhöht den arteriellen Blutdruck durch Vasokonstruktion, Stimulation der Aldosteronfreisetzung und nachfolgender Salzund Wasserretention. Plasma-Angiotensin wirkt darüberhinaus auf zentrale Mechanismen der Blutdruckregulation. Angiotensin ist ebenfalls im Gehirn vorhanden als Teil des endogenen Gehirnrenin-Angiotensin-Systems. Das Gehirn-Angiotensin wird nicht an das Blut abgegeben und kann als Neurohormon mit vorwiegend lokaler Funktion angesehen werden. Eine Beteiligung des Gehirn-Angiotensins an der Aufrechterhaltung des hohen Blutdruckes spontan hypertensiver Ratten ist nachgewiesen worden. Es bestehen Rückkoppelungen zwischen dem Plasma-Angiotensin auf der einen Seite und dem Gehirn-Angiotensin auf der anderen Seite. Stimulation von bestimmten, für die zentrale Blutdruckregulation bedeutsamen Hirnarealen beeinflußt die Reninsekretion von der Niere. Das Renin-Angiotensin-System (RAS) kann als ein Modell für die engen Zusammenhänge zwischen humoraler und neurohumoraler Blutdruckregulation angesehen werden.
    Type of Medium: Electronic Resource
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