Central effects of the?-adrenergic blocking agent acebutolol

1977 ◽  
Vol 12 (5) ◽  
pp. 327-331 ◽  
Author(s):  
K. Kayed ◽  
O. B. Godtlibsen
Keyword(s):  
Blocking Agent ◽  
Central Effects ◽  
Adrenergic Blocking

Nonstereoselective aspects of propranolol pharmacodynamics

1986 ◽  
Vol 64 (12) ◽  
pp. 1455-1462 ◽  
Author(s):  
M. Alkondon ◽  
A. Ray ◽  
P. Sen
Keyword(s):  
Inhibitory Action ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
The Body ◽  
Cholinergic Mechanism ◽  
Central Effects ◽  
Biochemical Studies ◽  
Β Blockers ◽  
Adrenergic Blocking ◽  
Therapeutic Profile

Twenty years after its discovery, the β-adrenergic blocking agent propranolol continues to interest pharmacologists and clinicians. Its therapeutic profile has extended to areas beyond the purview of the cardiovascular system, and its ocular and central nervous system effects have been well documented. In addition, it still remains a very good pharmacological tool to map out the adrenergic β-receptors in the body, and stereoisomers of propranolol and other β-blockers serve as valuable agents to distinguish between the effects related to β-adrenoceptors and those which are not. The primary purpose of this review is to summarize the evidence indicating that β-adrenergic blocking agents lack stereoselectivity in some of their effects, including several of considerable therapeutic importance. Because many pharmacological actions of propranolol followed a nonsteroselective pattern, the involvement of β-adrenoceptors in them was questioned and this led to the search for alternate mechanisms to explain these effects. Studies with propranolol and some related drugs indicated the involvement of a cholinergic mechanism in their antiarrhythmic, ocular hypotensive and some central effects. Also, a presynaptic inhibitory effect at the skeletal neuromuscular junction has been suggested to explain the benefical effect of propranolol and other β-blockers in tremor. Biochemical studies with these drugs revealed their inhibitory action on the cholinesterase enzyme in blood and other tissues like myocardium and brain. It is thus hypothesized that modulation of cholinergic neurotransmission by propranolol could explain some of its nonstereoselective actions and open new vistas in propranolol pharmacodynamics.

The central effects of the β-adrenergic blocking agent INPEA

1972 ◽  
Vol 11 (5) ◽  
pp. 609-614 ◽  
Author(s):  
R.Yu. Ilyutchenok ◽  
M.A. Gilinsky ◽  
A.G. Yeliseyeva ◽  
B.P. Jivotikoff ◽  
L.V. Loskutova ◽  
...  
Keyword(s):  
Blocking Agent ◽  
Central Effects ◽  
Adrenergic Blocking

Contribution of Adrenaline to the Fibrinolytic Activity Evoked by E. Coli Endotoxin in the Rat

1983 ◽  
Vol 50 (02) ◽  
pp. 557-559 ◽  
Author(s):  
J F Fracasso ◽  
A M Rothschild
Keyword(s):  
Fatty Acid ◽  
Adrenal Gland ◽  
Intravenous Injection ◽  
Fibrinolytic Activity ◽  
Blocking Agent ◽  
E Coli ◽  
Adrenergic Blocking

SummaryIntravenous injection of E. coli endotoxin (ETX), of adrenaline (AD) or of carbamylcholine (CBCH), caused fibrinolytic activity (FA), directly detectable on plasminogen-rich fibrin plates, to appear in the plasma of the rat. Adrenodemedul- lation abolished responses to ETX or CBCH, but enhanced those to AD. Rats given ETX exhibited marked hypotension, followed by a compensatory phase of normotension abolished by adrenodemedullation and significantly attenuated by phenoxy- benzamine, an a-adrenergic blocking agent which however failed to block FA caused by either ETX or AD. Aspirin, but not indomethacin, inhibited FA evoked by ETX, AD or CBCH. These results suggest that FA evoked by ETX in the rat is caused by AD released from the adrenal gland and does involve the fatty acid cyclooxygenase system.

ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura
Keyword(s):  
Intravenous Infusion ◽  
Human Subjects ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Glucose Levels ◽  
Alpha Receptors ◽  
Normal Human ◽  
Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

Massive Clonidine Ingestion with Hypertension in a 9-Month-Old Infant

PEDIATRICS ◽  
1983 ◽  
Vol 72 (4) ◽  
pp. 500-502
Author(s):  
Pablo Yagupsky ◽  
Rafael Gorodischer
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Drugs ◽  
Complete Recovery ◽  
Blocking Agent ◽  
Assisted Ventilation ◽  
Antagonistic Effect ◽  
Arterial Blood ◽  
Clonidine Poisoning ◽  
Adrenergic Blockers ◽  
Adrenergic Blocking

The antihypertensive drug clonidine has a double and antagonistic effect on arterial blood pressure. As a result of activation of peripheral α-adrenergic receptors, it causes a transient increase in blood pressure; by a central action it decreases sympathetic tone which results in sustained bradycardia and hypotension. Both central and peripheral effects are experimentally blocked by tolazoline, an α-adrenergic blocking agent. The toxic symptoms seen in clonidine poisoning are usually produced by the central effect. A case of severe clonidine poisoning in a 9-month-old infant is reported. The clinical picture included coma, miosis, apneic spells, bradycardia, and hypertension. Rapid and complete recovery was obtained with supportive treatment that included assisted ventilation. No adrenergic blockers or antihypertensive drugs were given. Use of tolazoline in cases of clonidine overdose in children remains controversial. Supportive measures alone may be adequate for even the most severe cases.

The Usefulness of Dapiprazole, an Alpha-Adrenergic Blocking Agent, in Pigmentary Glaucoma

1996 ◽  
Vol 27 (9) ◽  
pp. 806-809
Author(s):  
Leonardo Mastropasqua ◽  
Paolo Carpineto ◽  
Marco Ciancaglini ◽  
Pier Enrico Gallenga
Keyword(s):  
Blocking Agent ◽  
Pigmentary Glaucoma ◽  
Adrenergic Blocking

Cardiovascular responses to insulin in the absence of hypoglycemia

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud
Keyword(s):  
Pressor Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Right Atrial ◽  
Systemic Vein ◽  
Anesthetized Dogs ◽  
Adrenergic Blocking ◽  
The Brain

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.

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