Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serotonin (5-hydroxytryptamine; 5HT) kinetics and platelet activation by 5HT were studied in patients with essential hypertension (n = 45), and in matched normotensive subjects (n = 45). Platelet response to 5HT and plasma beta-thromboglobulin increased with age in men, both normotensives and hypertensives. Beta-thromboglobulin and 5-hydroxyindoleacetic acid (5HIAA) excretion were higher in hypertensive men than in women. In women, no changes in platelet activity or 5HIAA excretion were found. 5HT plasma concentrations increased with blood pressure. Platelet 5HT uptake (Vmax and KM) were the lowest in hypertensive men greater than or equal to 60 years of age. This may indicate that 5HT uptake in vivo in normotensives is far below maximum (VNT much less than Vmax), whereas in hypertensive men it may be close to maximum (VHT approximately Vmax). This could reflect significantly higher 5HT plasma concentrations in vivo hypertensives than in normotensives. The reduced uptake (which was found only in hypertensive men) may indicate an insufficient compensation of the enhanced 5HT release from aggregating platelets in older men, in whom platelet activity is enhanced in vivo. It is concluded that the defect in platelet 5HT uptake in hypertensives--along with the enhanced platelet aggregation--may contribute to a critical increase in 5HT plasma concentrations locally. An increase in 5HT concentrations leads to biochemical changes (higher 5HIAA excretion) as well as to an enhanced stimulation by 5HT. This may be of clinical relevance especially in older men, in whom 5HT2-receptor mediated responses are enhanced.
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PMID:Impaired uptake of 5 hydroxytryptamine platelet in essential hypertension: clinical relevance. 170 94

The effect of the calcium antagonist isradipine on serotonin metabolism and platelet aggregation was studied in 17 patients with essential hypertension. Platelet serotonin content, plasma serotonin, 5-hydroxyindoleacetic acid levels, and platelet aggregation [induced ex vivo by serotonin and low-density lipoprotein (LDL)] were measured after a 4-week placebo period and after 12 weeks of oral treatment with isradipine. Isradipine treatment significantly inhibited platelet aggregation induced by LDL and serotonin; the amplifying effect of LDL on serotonin-induced aggregation seen with placebo was not observed after 12 weeks of treatment with isradipine. Platelet serotonin content increased significantly during isradipine treatment; this increase was inversely related to the pretreatment content of serotonin in platelets. The results indicate that treatment with isradipine restores the impaired handling of platelet serotonin as well as the platelet response to serotonin and LDL in hypertensive patients. This effect of isradipine may be regarded as one of the cellular mechanisms of thrombovascular protection and may be of clinical significance in terms of platelet and vessel wall interaction.
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PMID:Serotonin and platelet activation during treatment with isradipine. 172 Apr 82

Concentrations of serotonin and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in platelet rich plasma, the urinary 5-HIAA excretion rate, and serotonin-induced platelet aggregation were measured in 17 patients with essential hypertension before, and at the end of, 8 weeks of oral ketanserin therapy at 20 to 40 mg twice daily. Ketanserin lowered systolic and diastolic blood pressure (p less than 0.01) and led to a reduction of serotonin concentration in platelet rich plasma in all patients (p = 0.05), as well as a decrease in 5-HIAA excretion rates in patients older than 55 years (p less than 0.05). Changes in 5-HIAA concentration in platelet rich plasma correlated with the fall in diastolic blood pressure (r = 0.67, p less than 0.05). Serotonin-induced platelet aggregation was inhibited by ketanserin (p less than 0.05), and this was more pronounced in older patients. Thus, antihypertensive therapy with ketanserin reduced platelet aggregation and serotonin metabolism in relation to the age of patients, and this may contribute to the reduction of their elevated rates of thromboembolic complications.
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PMID:Serotonin metabolism and age-related effects of antihypertensive therapy with ketanserin. 246 92

Five patients with essential hypertension who were receiving treatment with the beta- and alpha-adrenoreceptor-blocking drug labetalol had elevated urinary excretion of catecholamines. When measured with a radioenzymatic assay, all five subjects had elevated urinary excretion of norepinephrine and normal urinary excretion of epinephrine; when measured with a fluorometric assay, four subjects had elevated urinary excretion of epinephrine with normal urinary excretion of norepinephrine, and one subject had elevated urinary norepinephrine excretion with normal urinary excretion of epinephrine. In three subjects who could be reevaluated three days to two months after labetalol therapy was discontinued, the urinary catecholamine levels had returned toward normal. Our studies indicate that labetalol produced a false elevation of urinary catecholamine levels. Although labetalol also interfered with the measurement of urinary excretion of metanephrine, it did not interfere with the measurement of urinary excretion of vanillylmandelic acid, homovanillic acid, 5-hydroxyindoleacetic acid, and serotonin, and it probably did not interfere with the measurement of plasma concentrations of dopamine, norepinephrine, and epinephrine. We conclude that labetalol therapy should be discontinued, and another beta-blocking drug, such as propranolol, that does not interfere with these tests should be temporarily substituted at least three days before a patient collects a 24-hour urine for measurement of the urinary excretion of catecholamines and metanephrine.
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PMID:Falsely elevated urinary excretion of catecholamines and metanephrines in patients receiving labetalol therapy. 368 May 86