Antihypertensives

Scriabine, Alexander; Taylor, David G.

doi:10.1002/14356007.a04_235

Cited by 1 publication

(4 citation statements)

References 216 publications

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“…The attributed to the non-specific membrane-stabilizing activity (MSA) since the specific betablocking effect was without importance and the hydrophilic practo-101, a betablocker without MSA, had less platelet inhibitory effects (4,33,34). The lipophilic timolol maleate has very weak MSA (6,12,26). Thus, it is unlikely that the platelet-inhibitory effect obtained by timolol after a single dose can be explained by MSA which was suggested to be the mechanism for the platelet effect of propranolol (33).…”

Section: Discussionmentioning

confidence: 99%

“…The platelet-inhibiting effect of propranolol is dose dependent (30). Orally given timolol maleate is five to ten times more potent than propranolol in antagonizing the positive chronotropic effect of isoproterenol (26). Thus doses of 40 mg propranolol and 5 mg timolol should be expected to be equipotent from a betablocking point of view.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the effect of timolol on the occurrence of ventricular arrhythmias was not caused by any general effect on platelets. Antiarrhytmic properties of timolol have been reported in dogs (26). Timolol effectively prevented arrhythmias related to high levels of catecholamines.…”

Section: Adp-2 Thresholdmentioning

confidence: 95%

“…Timolol effectively prevented arrhythmias related to high levels of catecholamines. The betablocking effect of timolol may be responsible for the presently observed antiarrhythmic effect since MSA of timolol is negligible (12,26). However, resting values of catecholamines are low.…”

Section: Adp-2 Thresholdmentioning

confidence: 99%

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Effect of Timolol on Platelet Aggregation in Coronary Heart Disease

Thaulow

Kjekshus

Erikssen

1981

Journal of Internal Medicine

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The immediate effect of beta‐blockers versus placebo in platelet function was studied in ten healthy men one hour after either 40 mg propranolol, 5 mg timolol or placebo was given. Both beta‐blockers had similar platelet effects. They increased the ADP‐threshold in a platelet aggregation test and reduced the plasma level of beta‐thromboglobulin whereas the primary aggregation remained unchanged. Forty‐four patients were given timolol 10 mg twice daily or corresponding placebo medication in a secondary prevention trial after a myocardial infarction. At rest and also immediately after a near maximal exercise test the platelet function was similar on timolol and placebo. During exercise a lower ADP‐threshold and a higher plasma level of beta‐thromboglobulin was observed irrespective of whether the patients received placebo or timolol. Thus, the acute platelet inhibiting effect of timolol observed after a single dose disappeared during chronic timolol treatment. During 24 hours continuous ambulatory ECG monitoring patients on timolol treatment had significantly less arrhythmias than patients on placebo. A general effect on platelets cannot explain this antiarrhythmic effect of timolol during chronic therapy.

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