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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with essential hypertension and normal renal function were treated with ketanserin (20-40 mg twice a day), administered for 8 weeks. In all patients, the changes in systemic and renal hemodynamics, and in urine albumin excretion, were assessed. Ketanserin monotherapy effectively lowered blood pressure in all patients. No change in cardiac output, pulse rate and stroke volume was observed; peripheral vascular resistance was significantly decreased. Plasma volume was unaltered. Renal plasma flow, glomerular filtration rate and filtration fraction were stable, with a slight but not significant reduction in renal vascular resistance. Urine albumin excretion remained unchanged. No relevant side effects were observed during the treatment period. In conclusion, our results confirm that ketanserin alone is an effective antihypertensive agent in patients with uncomplicated essential hypertension. The blood pressure lowering effect is mainly due to the systemic vasodilatation; renal hemodynamics and function are well preserved.
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PMID:Antihypertensive therapy with ketanserin: effects on central and renal hemodynamics, and microalbuminuria. 230 49

Ketanserin, which preferentially blocks 5-HT2-serotonergic receptors, was injected intravenously (i.v.) to patients with congestive heart failure in a bolus dose of 10 mg, followed by an i.v. infusion of 3 mg/h over a period of 4 h. The drug caused a decrease in total peripheral resistance and, conversely, an increase in stroke volume. Right atrial and pulmonary artery pressures were decreased. Plasma noradrenaline rose twofold over the basal levels shortly after injection, but showed a distinct fall 2 h after beginning of the treatment. The concentrations of ketanserin in plasma after bolus injection approximated 100-150 ng/ml. The sympathoneuronal and sympathoadrenal reaction during tilting were increased after i.v. injection of 10 mg ketanserin in volunteers. The noradrenaline and adrenaline levels in plasma rose significantly more when compared with values before the injection of the drug. In vitro as well as in vivo ketanserin exerts a concentration-dependent inhibitory effect on the active transport of serotonin and catecholamines (dopamine, noradrenaline, adrenaline) into human platelets. Considering platelets as a model of the sympathetic neurons, the inhibition of reuptake of catecholamines by ketanserin could contribute to the observed increase in circulating catecholamines after injection of the drug.
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PMID:Effect of ketanserin on hemodynamics, plasma-catecholamine concentrations, and serotonin uptake by platelets in volunteers and patients with congestive heart failure. 241 24

Ketanserin (120 mg/day) or placebo was given orally to 14 patients with mild to moderate essential hypertension according to a double-blind crossover protocol, each treatment period lasting 6 weeks. Resting intraarterial pressure in the recumbent position was reduced from 150/84 to 141/77 mm Hg; the hypotensive effect persisted throughout an uninterrupted graded exercise test to the point of exhaustion. The hemodynamic effects were similar at rest and during exercise. Overall, systemic vascular resistance decreased by 14%, heart rate fell by 5%, but stroke volume and cardiac output increased. The pressor responses to methoxamine and to phenylephrine were reduced by ketanserin.
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PMID:Hemodynamic response to chronic ketanserin treatment in essential hypertension. 241 34

Pulmonary embolism may cause pulmonary hypertension by mechanical obstruction, which might be amplified by vasoconstriction induced by serotonin released from the emboli. The purpose of the present study was to examine whether 5-HT2-receptors are involved in serotonin-induced pulmonary hypertension. Ketanserin was used as 5-HT2-serotonergic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 micrograms/kg . min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmax), heart rate (HR), and mean aortic pressure (PAO) was studied with and without treatment by ketanserin (20 and 100 micrograms/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmax. A dose of 20 micrograms/kg ketanserin did not affect hemodynamics significantly, whereas 100 micrograms/kg of the compound significantly reduced PAO, TPR, and left ventricular dP/dtmax. The serotonin-induced increases in PAP, PVR, dP/dtmax, CO, and SV were reduced significantly by 100 micrograms/kg ketanserin; the lower dose of ketanserin had only a slight blocking effect. Ketanserin blocks serotonin-induced pulmonary vasoconstriction partly, but it seems also to antagonize the positive inotropic effect of the monoamine.
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PMID:Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin. 241 62

Ketanserin, a selective serotonergic (5-HT2) antagonist, also has affinity for alpha 1-adrenoceptors. It is not clear whether the hypotensive mechanism of ketanserin is due to its antagonistic action to 5-HT2 receptor or to its affinity for alpha 1 adrenoceptors. The hypotensive mechanism of ketanserin was studied in both stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY). Anesthetized rats were used (alpha-chloralose + urethane, i.p.). Up to 3 ml of blood was drawn from each rat for analysis. Plasma norepinephrine (NE) was determined by radioenzymatic assay. Plasma serotonin (5-HT) was determined by HPLC-ECD. Adrenal nerve discharges were counted by a digital pulse counter. Ketanserin (0.5 mg/kg, 5.0 mg/kg, i.v.) produced a dose-dependent reduction of mean arterial pressure (MAP) in both SHRSP and WKY. MAP of SHRSP decreased significantly as compared with WKY. Both plasma NE and 5-HT showed a tendency to increase during ketanserin administration (5.0 mg/kg, i.v.). Ketanserin significantly antagonized the BP response induced by exogenously injected 5-HT (30 micrograms/kg) and NE (10 micrograms/kg). Adrenal nerve activity was reduced in parallel with the decrease in BP and HR. These findings suggest that ketanserin produced a decrease in BP via both peripheral and central action in rats.
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PMID:[Effect of ketanserin on blood pressure in rats]. 241 29

The cardiovascular effects of ketanserin (5-HT2-receptor antagonist with alpha 1-receptor blocking property) were studied during coronary artery surgery. Sixteen patients were anesthetized with flunitrazepamfentanyl-nitrous oxide-oxygen-pancuronium. Ketanserin (10 mg i.v.) was used to decrease elevated blood pressure unresponsive to deepening of anesthesia before extracorporeal circulation. Ketanserin caused a marked vasodilation in all patients, significant (p less than 0.05) decreases of systolic, diastolic, and mean arterial blood pressure, and of pulmonary artery pressure and pulmonary capillary wedge pressure. As a result, indirect indices of myocardial oxygen demand (rate-pressure product and "triple index") also decreased. Heart rate and right atrial pressure remained unchanged, while cardiac index and stroke volume index increased slightly. Ketanserin was found to be effective in the treatment of prebypass hypertension; the elevated blood pressure returned to normal; unwanted hypotension was not observed.
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PMID:Cardiovascular effects of ketanserin in the treatment of hypertension during coronary artery bypass surgery. 241 72

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 h), blood pressures measured 12 h after dosing were not significantly different from those obtained during the placebo period. However, 2 h after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (p less than 0.01) and 6 +/- 5 mm Hg (p less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. At the time of peak antihypertensive activity, plasma renin activity, aldosterone, growth hormone, and prolactin levels were unchanged. Prolactin levels decreased slightly (4.1 +/- 3.0 vs. 3.7 +/- 2.9 ng/ml, p less than 0.05) during ketanserin therapy when measured 12 h after dosing. Other pituitary hormones, serum testosterone, plasma catecholamines, and plasma lipids showed no changes. Heart rate was also unchanged. Stroke volume, measured 2 h after dosing, increased (70 +/- 22 vs. 85 +/- 31 ml, p less than 0.05) with ketanserin therapy, but cardiac output did not change significantly. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24-h antihypertensive activity.
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PMID:Antihypertensive therapy with ketanserin: metabolic and hemodynamic effects. 246 37

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 hours), blood pressures measured 12 hours after dosing were not significantly different from those obtained after placebo. However, 2 hours after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (P less than 0.01) and 6 +/- 5 mm Hg (P less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. Except for a slight decline in serum prolactin levels 12 hours after dosing with ketanserin, no changes were observed in pituitary hormone levels, serum testosterone, plasma catecholamines, plasma renin activity, aldosterone, or lipoproteins. Stroke volume, measured 2 hours after dosing, increased with ketanserin therapy, but cardiac output, systemic resistance, and heart rate were unchanged. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24 hours of antihypertensive activity.
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PMID:Metabolic and hemodynamic effects of antihypertensive treatment with ketanserin. 341 1

Ketanserin (R 41 468), a quinazoline derivative, has been shown to be a selective blocker of 5-HT2 receptors. The drug was administered intravenously (10 mg given over a 3 min period) to 8 patients with severe cardiac failure already treated with digitalis, diuretics, and, in 4 cases, vasodilators. R 41 468 produced a significant fall in right-atrial, pulmonary-artery, pulmonary-wedge, and systemic arterial pressures. Systemic dynamic and total pulmonary vascular resistances were also reduced. Cardiac and stroke-work indices both increased, Heart rate remained unchanged. The platelet aggregation index, assessed in 2 patients, was initially low and was nearly normal 15 min after administration of a single dose of R 41 468.
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PMID:5-HT2-receptor blockade in the treatment of heart failure. A preliminary study. 611 31

Ketanserin (120 mg/day) or placebo was given orally to 14 patients with mild to moderate essential hypertension according to a double blind crossover protocol, each treatment period lasting six weeks. Resting intra-arterial pressure in the recumbent position was reduced from 150/84 to 141/77 mm Hg; the hypotensive effect persisted throughout an uninterrupted graded exercise test to the point of exhaustion. The haemodynamic effects were similar at rest and during exercise. Overall, systemic vascular resistance decreased by 14%, heart rate fell by 5%, but stroke volume and cardiac output increased. Mean pulmonary arterial pressure and capillary wedge pressure were not significantly affected, but pulmonary vascular resistance decreased by 15%. The pressor response to methoxamine was significantly reduced by ketanserin. Both plasma noradrenaline and adrenaline concentrations increased, plasma renin activity and angiotensin II concentration decreased, and plasma aldosterone concentration was unchanged. The data indicate that ketanserin induces arteriolar dilatation, possibly related to an alpha-1-antagonistic action and to a reduced circulating angiotensin II concentration. The haemodynamic response is complex, and an increase in cardiac output limits the hypotensive effect. There is no firm evidence of an effect on venous tone as cardiac filling pressures do not change.
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PMID:Haemodynamic and humoral responses to chronic ketanserin treatment in essential hypertension. 636 88


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