Autonomic drugs used in the treatment of the hypertensive patient with particular reference to beta-receptor blocking agents

Author(s):  
Andrew J. Lonigro
1974 ◽  
Vol 35 (2) ◽  
pp. 272-280 ◽  
Author(s):  
CHANG-SENG LIANG ◽  
WILLIAM B. HOOD

1988 ◽  
Vol 22 (6) ◽  
pp. 484-485 ◽  
Author(s):  
Gopal Das ◽  
Janine C. Ferris

Beta-receptor blocking agents are commonly used to treat patients with heart disease, and generalized seizures due to therapy with these agents are rare. All reported cases of seizures due to beta blocking agents have occurred only in those subjects who ingested large doses of the drugs. We observed generalized convulsions in a patient who was receiving therapeutic doses of an ultrashort-acting beta-blocking agent (esmolol hydrochloride) intravenously. A literature survey and possible mechanisms by which these agents induce seizures are presented.


1965 ◽  
Vol 209 (3) ◽  
pp. 539-544 ◽  
Author(s):  
J. A. Krasney ◽  
F. T. Paudler ◽  
D. C. Smith ◽  
L. D. Davis ◽  
W. B. Youmans

The cardioaccelerator influence of synthetic angiotensin observed in dogs having baroreceptors denervated or blood pressure buffered was studied. In dogs which had received morphine (3 mg/kg) and chloralose (90 mg/kg) and which had the sinoaortic zones denervated, angiotensin, in doses of 1 µg/kg intravenously, still caused cardiac acceleration after transection of the spinal cord at C6 or C7 or after removal of sym-pathetic chains bilaterally from the stellate through T4 or T5. In intact dogs under morphine-chloralose which had received full ganglionic blocking doses of either tetraethylammonium chloride or pentolinium tartrate, angiotensin produced marked cardiac acceleration. Administration of bretylium tosylate, in doses of 10 mg/kg intravenously, largely or completely prevented the cardioaccelerator action of angiotensin. The beta receptor blocking agents nethalide and Inderal had effects similar to those of bretylium tosylate. The studies indicate that there is a peripheral adrenergic basis for much or all of the cardiac acceleration produced by these doses of angiotensin. In the intact animal this influence would be expected to counteract much of the cardiac inhibition elicited reflexly from baroreceptors.


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