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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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