The Action of Beta-Receptor Blocking Agents on Cardiac Muscle

2015 ◽  
pp. 118-126 ◽  
Author(s):  
E. M. Vaughan Williams
Keyword(s):  
Cardiac Muscle ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor

scholarly journals The Myocardial Depressant Effect of Beta-Receptor Blocking Agents

1974 ◽  
Vol 35 (2) ◽  
pp. 272-280 ◽  
Author(s):  
CHANG-SENG LIANG ◽  
WILLIAM B. HOOD
Keyword(s):  
Depressant Effect ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor

Haemodynamic effects of the beta-receptor blocking agents metoprolol and propranolol in the anaesthetized dog

1978 ◽  
Vol 56 (S1) ◽  
pp. 107-112 ◽  
Author(s):  
H. Brunner ◽  
J. Gelzer ◽  
J. Stepanek
Keyword(s):  
Haemodynamic Effects ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor ◽  
Anaesthetized Dog

Generalized Convulsions in a Patient Receiving Ultrashort-Acting Beta-Blocker Infusion

1988 ◽  
Vol 22 (6) ◽  
pp. 484-485 ◽  
Author(s):  
Gopal Das ◽  
Janine C. Ferris
Keyword(s):  
Heart Disease ◽  
Beta Blocker ◽  
Blocking Agent ◽  
Literature Survey ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor ◽  
Generalized Seizures ◽  
Beta Blocking ◽  
Therapeutic Doses

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.

Haemodynamic effects of the optical isomers of beta-receptor blocking agents

1983 ◽  
Vol 4 (suppl D) ◽  
pp. 27-30 ◽  
Author(s):  
K. H. Rahn
Keyword(s):  
Haemodynamic Effects ◽  
Optical Isomers ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor

Mechanisms of cardioaccelerator action of angiotensin

1965 ◽  
Vol 209 (3) ◽  
pp. 539-544 ◽  
Author(s):  
J. A. Krasney ◽  
F. T. Paudler ◽  
D. C. Smith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Intact Animal ◽  
Tetraethylammonium Chloride ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Beta Receptor ◽  
Ganglionic Blocking

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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