Continuous Inhibition of Serotonin-Induced Platelet Aggregation during Chronic Ketanserin Administration to Man Can Be Detected after Plasma pH Control

Arnout, Jozef; Russelt, M Van; Deckmyn, Hans; Vermylen, J.

doi:10.1159/000215768

Cited by 2 publications

(2 citation statements)

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“…The ability of ketanserin to block 5-HT2 receptors therefore suggests that platelet-derived serotonin might be involved in the mechanism leading to posttransplant arteriosclerosis. Serotonin-mediated platelet aggregation has been demonstrated to be reduced by ketanserin (16,17). In the present study, the sensitivity of BN platelets was also reduced to low concentrations of collagen after ketanserin treatment.…”

Section: Discussionsupporting

confidence: 64%

“…Last, serotonin may stimulate arteriosclerosis by its conceptive role in chronic hypertension (15). Indeed, blocking the serotonin-2 (5-HT2) receptors by ketanserin, clinically applied as an antihypertensive agent, effectively antagonizes these effects of serotonin (16)(17)(18). Therefore, ketanserin has been suggested to provide protection to arteriosclerotic diseases (19).…”

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confidence: 99%

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Ketanserin Reduces Graft Arteriosclerosis After Allogeneic Aorta Transplantation in Rats

Geerling

Bruin²,

Scheringa³

et al. 1996

Journal of Cardiovascular Pharmacology

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The serotonin-2 receptor antagonist ketanserin has been suggested to diminish arteriosclerotic development by its effect on platelet function and on vascular smooth muscle cells. We investigated the ability of ketanserin in reducing immune-mediated arteriosclerosis using the BN-WAG and WAG-BN rat aortic transplantation models. Ketanserin (10 mg/kg/day) administered in drinking water significantly reduced posttransplant arteriosclerotic thickening of the intima in the BN-WAG rat model to 102 +/- 23 mu m as compared with 171 +/- 60 mu m in untreated BN-WAG allografts 8 weeks posttransplantation (p < 0.05). In the opposite WAG-BN combination, at 4 weeks posttransplantation, no significant reduction in intimal thickening was attained (112 +/- 42 vs. 152 +/- 49 mu m). Platelet aggregation to increasing amounts of collagen did not show a correlation between the effect of ketanserin on platelet function and reduction in intimal thickening. Ketanserin had no effect on systolic blood pressure or mononuclear cell infiltration. We conclude that ketanserin reduces graft arteriosclerosis by a mechanism other than by inhibition of platelet function, decrease in blood pressure, or immunosuppression. Because of this antiarteriosclerotic effect, ketanserin therapy might be beneficial to the long-term survival of vascular allografts.

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Section: Discussionsupporting

confidence: 64%

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confidence: 99%

Ketanserin Reduces Graft Arteriosclerosis After Allogeneic Aorta Transplantation in Rats

Geerling

Bruin²,

Scheringa³

et al. 1996

Journal of Cardiovascular Pharmacology

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Ketanserin

Brogden¹,

Sorkin²

1990

Drugs

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Ketanserin is a 5-HT2 receptor antagonist without partial agonist properties which also possesses weak alpha 1-adrenoceptor antagonistic activity, which may explain its antihypertensive mechanism of action in patients with essential hypertension. It also inhibits the effects of serotonin on platelets in cardiovascular disease, inhibits vasoconstriction caused by the amine, and when administered intravenously improves some haemorheological indices in patients with ischaemic diseases. The antihypertensive effect of oral ketanserin 40 mg twice daily is comparable with that of total daily doses of metoprolol 200 mg, propranolol 160 mg, captopril 100 mg, enalapril 20 mg, hydrochlorothiazide 50 mg, or alpha-methyldopa 1000 mg and is achieved without adverse effect on plasma lipoproteins or carbohydrate metabolism in patients with concomitant diabetes mellitus. Evidence from prospective studies suggests a greater antihypertensive efficacy in the elderly than in younger patients. In patients with intermittent claudication, results have been inconsistent in small studies, while a large study showed no improvement in pain-free walking distance but fewer amputations compared to placebo. In Raynaud's phenomenon symptomatic improvement relative to placebo was achieved in larger trials. Its role in preventing atherosclerotic complications requires further investigation. Ketanserin is reasonably well tolerated, the frequency of adverse effects being comparable with that of other antihypertensive drugs in controlled trials. Dizziness, tiredness, oedema, dry mouth and weight gain are the most commonly reported effects. Ketanserin prolongs QT interval in a dose-related manner, and when given in certain predisposing circumstances ventricular arrhythmias and syncope may occur. Administered intravenously, ketanserin 10mg followed by an infusion of 2 to 4 mg/h controls moderate to severe pre- and postoperative hypertension in most patients, acting as a balanced vasodilator, lowering cardiac pre- and afterload. Although the arrhythmogenic potential of ketanserin in patients receiving potassium-depleting diuretics requires suitable precautions, it appears that its antihypertensive activity is suited to the elderly provided plasma potassium concentrations are normal at the start of treatment and are maintained within the normal range.

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Continuous Inhibition of Serotonin-Induced Platelet Aggregation during Chronic Ketanserin Administration to Man Can Be Detected after Plasma pH Control

Cited by 2 publications

References 10 publications

Ketanserin Reduces Graft Arteriosclerosis After Allogeneic Aorta Transplantation in Rats

Ketanserin Reduces Graft Arteriosclerosis After Allogeneic Aorta Transplantation in Rats

Ketanserin

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