Increased platelet adhesion and aggregation in hypertensive patients: effect of atenolol.

Markel, A.; Brook, J.G.; Levy, Yishai; Aviram, Michael; Youdim, M.B.H.

doi:10.1111/j.1365-2125.1983.tb02238.x

Cited by 17 publications

(7 citation statements)

References 32 publications

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“…β-blockers have been demonstrated to decrease platelet aggregation and adhesion. [ 30 ] The action of β-blocker is likely to be by multiple mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of use of β-blockers in sepsis

Chacko

Gopal

2015

J Anaesthesiol Clin Pharmacol

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Background and Aims:We proposed a review of present literature and systematic analysis of present literature to summarize the evidence on the use of β-blockers on the outcome of a patient with severe sepsis and septic shock.Material and Methods:Medline, EMBASE, Cochrane Library were searched from 1946 to December 2013. The bibliography of all relevant articles was hand searched. Full-text search of the grey literature was done through the medical institution database. The database search identified a total of 1241 possible studies. The citation list was hand searched by both the authors. A total of 9 studies were identified.Results:Most studies found a benefit from β-blocker administration in sepsis. This included improved heart rate (HR) control, decreased mortality and improvement in acid-base parameters. Chronic β-blocker usage in sepsis was also associated with improved mortality. The administration of β-blockers during sepsis was associated with better control of HR. The methodological quality of all the included studies, however, was poor.Conclusion:There is insufficient evidence to justify the routine use of β-blockers in sepsis. A large adequately powered multi-centered randomized controlled clinical trial is required to address the question on the efficacy of β-blocker usage in sepsis. This trial should also consider a number of important questions including the choice of β-blocker used, optimal dosing, timing of intervention, duration of intervention and discontinuation of the drug. Until such time based on the available evidence, there is no place for the use of β-blockers in sepsis in current clinical practice.

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“…β-blockers have been demonstrated to decrease platelet aggregation and adhesion. [ 30 ] The action of β-blocker is likely to be by multiple mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of use of β-blockers in sepsis

Chacko

Gopal

2015

J Anaesthesiol Clin Pharmacol

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“…Furthermore, there may be a relationship between the accumulation of atenolol in the platelet and the reduced platelet adhesion which it causes. 27…”

Section: Discussionmentioning

confidence: 99%

Stereoselective accumulation of the β‐receptor blocking drug atenolol by human platelets

Walle¹,

Webb²,

Walle³

et al. 1991

Chirality

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We have studied the stereochemistry of accumulation of the hydrophilic beta-adrenoceptor antagonist rac-atenolol by human platelets in vitro. The accumulation was slow, not reaching equilibrium until 90 min at 37 degrees C. The uptake was temperature dependent with the accumulation at 37 degrees C being 3-4 times greater than at 4 degrees C. The accumulation was also stereoselective at 37 degrees C, favoring the active (-)-enantiomer over the (+)-enantiomer by 2.3-fold. Reserpine, but not desipramine, inhibited the platelet accumulation of rac-atenolol enantiospecifically. This uptake profile is different from the platelet uptake of lipophilic beta-blockers, which is characterized by nonspecific membrane binding, but similar to the carrier-mediated accumulation of the neurotransmitter norepinephrine by storage granules within the platelet.

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“…Endogenous serotonin released from platelets can cause systemic vasocon striction and elevation of blood pressure and stimulation of platelet aggregation. Propran olol, the original P-blocker drug, which is not cardiosclective [24], and atenolol, a specific Pi-receptor blocker [25], have been estab lished as effective antihypertensive drugs, and both drugs effectively decrease platelet aggregation [25], We have demonstrated that both drugs also depress platelet adhesion, even though the appearance of this inhibition took longer than the decrement in blood pressure. This may suggest either that the reduction in blood pressure is not the only parameter affecting platelet adhesion in these patients or that the depressed platelet adhe sion is a consequence of some process (reduc tion in catecholamines) that follows the fall in blood pressure.…”

Section: ]-mentioning

confidence: 98%

Platelet Adhesion in Hyperlipidemic and Hypertensive Patients

Brook¹,

Marmur²,

Berkovitch³

et al. 1985

Pathophysiol Haemos Thromb

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Platelet adhesion was studied in whole blood using a simple stagnation flow method in patients at high risk for the development of atherosclerosis. Fourteen patients with hypercholesterolemia, 26 with hypertriglyceridemia and 25 normolipidemic hypertensive subjects were compared with 75 normal (normotensive and normolipidemic) subjects. Increased platelet adhesion was found in hypercholesterolemic (but not hypertriglyceridemic) patients only when native blood with no anticoagulants was used. In hypertensive patients, platelet adhesion was signficantly elevated, but remarkably reduced by beta-blocker drugs. Propranolol and atenolol significantly reduced platelet adhesion, but this effect was found to take a longer time than that required for significant blood pressure reduction.

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Increased platelet adhesion and aggregation in hypertensive patients: effect of atenolol.

Cited by 17 publications

References 32 publications

Systematic review of use of β-blockers in sepsis

Systematic review of use of β-blockers in sepsis

Stereoselective accumulation of the β‐receptor blocking drug atenolol by human platelets

Platelet Adhesion in Hyperlipidemic and Hypertensive Patients

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