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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether platelet response to mental stress is altered in essential hypertension, platelet aggregability and plasma beta-thromboglobulin were determined in 24 patients with essential hypertension (11 patients with World Health Organization (WHO) stage I and 13 patients with stage II) and 14 normotensive controls before and after a 10-min arithmetic stress (serial subtraction of 7 from 1000). In normotensive subjects, arithmetic stress did not affect primary aggregations to 1.0 micromol/L adenosine diphosphate (ADP) and to 2.5 micromol/L 5-hydroxytryptamine (5-HT), ADP threshold for biphasic aggregation and plasma beta-thromboglobulin level. In hypertensive patients with WHO stage I, these parameters were similar to those in normotensives before arithmetic stress, but the arithmetic stress test significantly increased primary aggregation to reagents and beta-thromboglobulin level, and decreased threshold of ADP for biphasic aggregation. In WHO stage II patients, platelet aggregability to reagents and beta-thromboglobulin level were already enhanced as compared with WHO stage I patients and normotensive subjects before arithmetic stress. However, the stress-induced changes in platelet function were less pronounced in WHO stage II patients compared with stage I patients. In conclusion, platelet aggregability and proaggregatory effect of mental stress differed depending on the severity of hypertension in patients with essential hypertension; the transient activation of platelet function during stress with no enhancement under the resting condition in the early phase of hypertension and the continuous activation of platelet function in the advanced phase with hypertensive organ damage.
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PMID:Different platelet aggregability during mental stress in two stages of essential hypertension. 1060 81

To evaluate the effect of antihypertensive therapy on platelet activation in essential hypertension, the plasma levels of beta-thromboglobulin (beta-TG) were examined in 45 patients with essential hypertension and 20 age-matched normotensive control subjects. Hypertensive patients were assigned to monotherapy with one of five different antihypertensive drugs for 6 months, and the change of plasma levels of beta-TG was reexamined after the completion of the monotherapy. The plasma beta-TG increased in hypertensive patients compared with levels in normotensive control subjects. Monotherapy with each drug resulted in sufficient blood pressure control in all hypertensive patients. The plasma beta-TG decreased significantly after monotherapy with an alpha-blocker or an angiotensin-converting enzyme inhibitor (ACEI). The plasma beta-TG increased with the use of a diuretic but did not change with the use of a beta-blocker or calcium antagonist. The platelet activation observed in patients with essential hypertension is reversed by monotherapy with an alpha-blocker or an ACEI. It is possible that these drugs reduce the development of hypertensive vascular complications due to suppression of platelet activation in patients with essential hypertension.
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PMID:Effects of antihypertensive treatment on platelet function in essential hypertension. 1113 Dec 67

In patients with essential hypertension, increased level of platelet activity expressed as the concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were observed. Elevation of the levels of both beta-TG and PF4 correlated with the increase in platelet aggregability in platelet-rich plasma (PRP) and the decrease in red blood cell deformability, which were considered as being the possible factors for the platelet intravascular activation. After 2 weeks of monotherapy with nifedipine (40 mg daily), a decrease in platelet aggregability in PRP was observed in 35 of the 75 patients and an increase in red cell deformability in 37 of the 75 patients. Using cluster analysis, all cases were divided into several groups based on nifedipine effects on red cell deformability and platelet aggregability in PRP. It was revealed that the statistically significant decrease in the levels of platelet markers took place only in patients in whom nifedipine simultaneously decreased platelet aggregability and increased red cell deformability. Analysis of variance showed a high power of influence for combined changes in these parameters for reducing intravascular platelet activation by nifedipine. It is suggested that nifedipine reduces platelet activity by direct action on platelets and indirectly due to its capacity to increase red cell deformability, resulting in elimination of platelet stimulation by red blood cells.
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PMID:Antiplatelet Effect of Nifedipine depending on its Action on Red Cell Deformability in Essential Hypertension. 1185 Jun 41

The aim of the study was to investigate the effect of therapy by rilmenidine on endothelial and platelet function in 23 patients with the early stages of untreated essential hypertension. The measurements were carried out before therapy, after 1 week of placebo administration, after 1 week, after 1 month and after 3 months of therapy. After 1 week of therapy both systolic (SBP) and diastolic blood pressure (DBP) were reduced (P < 0.001) all over the study period. Plasma thrombomodulin (TM) and von Willebrand factor (vWF) as indicators of endothelial dysfunction, and plasma beta-thromboglobulin (betaTG) as an indicator of in vivo platelet activation, were investigated. Fibrinogen as a risk factor for vascular changes was also assayed. Platelet aggregation without stimulation (spontaneous, SPA) and induced by adrenaline (APA) was measured. A decrease of plasma vWF level after 1 month (P < 0.05) and after 3 months (P < 0.05) of therapy was observed. We failed to find any changes of plasma TM and fibrinogen level. A reduction of platelet aggregation was evident after 1 week (SPA and APA, P < 0.05, respectively) but mainly after 1 month (SPA P < 0.01, APA P < 0.05) and after 3 months of therapy (SPA and APA, P < 0.01, respectively). It was accompanied by a decrease of plasma betaTG level after 3 months of therapy (P < 0.05). The vasculoprotective and antiplatelet effect of rilmenidine may be important in terms of the favourable role of antihypertensive drugs in cardiovascular morbidity.
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PMID:Effect of the new centrally acting antihypertensive agent rilmenidine on endothelial and platelet function in essential hypertension. 1214 57

Endothelial damage and platelet hyperactivity may play a role in the vascular complications of essential hypertension. Restoration of endothelial function and reduction of increased platelet aggregation in essential hypertension are one of the aims of modern anti-hypertensive therapy. Therefore, the effect of angiotensin converting enzyme (ACE) inhibitors on endothelial and platelet functions is of interest. In the present study, 23 healthy normotensives and 23 age- and sex-matched patients with non-treated essential hypertension (1st and 2nd stage according to WHO) were investigated. Measurements of endothelial and platelet functions in hypertensives were carried out before therapy, after 1 week of placebo administration, after 1 week and after 1 month of perindopril therapy in a once daily dose of 4 mg. Plasma thrombomodulin (ELISA method) and beta-thromboglobulin (radio immunoassay method) were assayed and platelet aggregation (spontaneous and induced by adrenaline) was measured. The values of plasma thrombomodulin, a novel marker of endothelial function, were compared between age- and sex-matched normotensives and hypertensives. A significant decrease of adrenaline-induced platelet aggregation was observed after 1 month of perindopril therapy in comparison with the values before therapy or after 1 week of perindopril therapy ( P < 0.02 and P < 0.05 respectively). There were no significant changes in plasma thrombomodulin or beta-thromboglobulin following therapy. We failed to find significant changes of plasma thrombomodulin in patients in the early stages of hypertension, but its tendency to be higher than in normotensives does not rule out some vascular damage. The inhibitory effect of perindopril on platelet aggregation may be a further advantage of this drug. Since no changes were found after 1 week of therapy, the reduction of adrenaline-induced platelet aggregation after 1 month of therapy may be explained by an indirect effect of perindopril on platelet function, probably asa result of protective action on the arterial wall.
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PMID:Effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril on endothelial and platelet functions in essential hypertension. 1679 47

Essential hypertension (EH) is a major risk factor for cardiovascular disease. Despite considerable efforts to elucidate the pathogenesis of EH, there is an imperious need for novel indicators of EH. This study aimed to develop a method to predict potential biomarkers of EH from the point of view of network. A pathway-based gene-gene interaction (GGI) network model was constructed and analyzed, containing 116 nodes and 1272 connections. The nodes represented EH-related genes, and that connections represented their interactions. The network showed a small-world property and uneven degree distribution, suggesting that a few highly interconnected hubs played a vital role in EH. An inherent hierarchy and assortative mixing pattern were also observed in the network. GNAS, GNB3, PF4 and PPBP showed the highest values of degrees and centrality indices, and were chosen as potential biomarkers of EH. A two-mode network model based on the potential biomarkers demonstrated that hemostasis and GPCR ligand binding pathway were key pathways contributing to EH. Results of this study improve our current understanding of the molecular mechanisms driving EH. The selected genes and pathways have the potential to be used in the diagnosis and treatment of EH. Moreover, the combination of pathway analysis and complex network methodology provides a novel strategy for searching new genetic indicators of complex diseases.
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PMID:Pathway-based gene-gene interaction network modelling to predict potential biomarkers of essential hypertension. 3011 May 99


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