Stimulation of calcium pump activity in heart sarcolemma by timolol

1983 ◽  
Vol 61 (3) ◽  
pp. 240-244 ◽  
Author(s):  
Andre Dzurba ◽  
Pallab K. Ganguly ◽  
Robert E. Beamish ◽  
Naranjan S. Dhalla
Keyword(s):  
Membrane Fluidity ◽  
Concanavalin A ◽  
Rat Heart ◽  
Calcium Pump ◽  
Blocking Agents ◽  
Heart Sarcolemma ◽  
Pump Activity ◽  
Adrenergic Blocking ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

The effects of β-adrenergic blocking agents, timolol and atenolol (1–1000 μM), were studied on rat heart sarcolemmal ATPase and Ca2+ binding activities. Timolol, unlike atenolol, increased both Ca2+-stimulated ATPase and ATP-dependent Ca2+ binding; the maximal effects were seen at 1 μM concentration of timolol. Both timolol and atenolol did not alter the sarcolemmal Mg2+ ATPase and nonspecific Ca2+ binding activities. Sarcolemmal Ca2+ -stimulated ATPase was also activated by concanavalin A (6–66 μg/mL) which is known to alter membrane fluidity; however, Mg2+ ATPase was unaffected by this agent. These results indicate that timolol may stimulate Ca2+ pump activity in heart sarcolemma by changing membrane fluidity in a manner similar to that of concanavalin A.

scholarly journals Comparative studies on effects of β-adrenergic blocking agents, quinidine and lidocaine on rat heart muscles

1975 ◽  
Vol 25 ◽  
pp. 67-68
Author(s):  
Mitsuhiro Nagata ◽  
Jun’o Shimamoto ◽  
Hiroko Murakami ◽  
Jiro Sugimoto ◽  
Masao Morita
Keyword(s):  
Comparative Studies ◽  
Rat Heart ◽  
Blocking Agents ◽  
Adrenergic Blocking ◽  
Adrenergic Blocking Agents

Effect of Adrenergic Blocking Agents on the Calcium Pump of the Fragmented Cardiac Sarcoplasmic Reticulum

Nature ◽  
1968 ◽  
Vol 220 (5162) ◽  
pp. 79-80 ◽  
Author(s):  
MICHAEL L. HESS ◽  
F. NORMAN BRIGGS ◽  
ELLIOT SHINEBOURNE ◽  
JOHN HAMER
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Pump ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Blocking Agents ◽  
Adrenergic Blocking ◽  
Adrenergic Blocking Agents

Liberation of antidiuretic hormone: pharmacologic blockade of ascending pathways

1964 ◽  
Vol 207 (6) ◽  
pp. 1405-1410 ◽  
Author(s):  
Elliott Mills ◽  
S. C. Wang
Keyword(s):  
Brain Stem ◽  
Ulnar Nerve ◽  
Nociceptive Response ◽  
Water Diuresis ◽  
Blocking Agents ◽  
Ascending Pathways ◽  
Adrenergic Blocking ◽  
The Brain ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

Water diuresis was established and maintained in dogs anesthetized with chloralose. Both ureters were cannulated and a continuous recording of urine flow obtained. ADH release was obtained from stimulation of the central end of a vagus nerve (the vagus-pituitary reflex), and ulnar nerve (nociceptive response) as well as from stimulation of reactive areas in the brain stem. Meperidine (10–15 mg/kg) and morphine (1–4 mg/kg) blocked the response to ulnar nerve stimulation and some brain-stem responses, but not the vagus-pituitary reflex. Similarly, the adrenergic blocking agents, Hydergine (0.3–0.6 mg/kg), phenoxybenzamine (2.0 mg/kg) and phentolamine (0.25 mg/ kg) markedly reduced the ulnar response and some brain-stem responses but not the vagus-pituitary reflex. However, larger doses of phenoxybenzamine (5 mg/kg) and Hydergine (1 mg/ kg) did inhibit the vagus-pituitary reflex. The anticholinergic agents, atropine (1–10 mg/kg) and ethybenztropine (0.5–2.0 mg/kg), were not effective blocking agents themselves but did render the inhibitory action of the adrenergic blocking agents more effective. These results suggest the existence of at least two different ascending pathways for ADH liberation. In addition, the evidence is compatible with the participation of adrenergic as well as cholinergic mechanisms in ADH liberation.

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