Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

In this study the authors examine whether smoking further heightens platelet activity and reduces fibrinolysis above that already present in mild hypertension. Ten smokers and 11 non-smokers, all with mild hypertension (defined as a diastolic pressure between 90 and 110 mm Hg) were compared for their platelet activity in vitro and in vivo and for their fibrinolytic activity. Successive measurements were made with the patients lying at rest after they had assumed the erect posture for 10 min and at the end of a 5-min moderately strenuous exercise test. The threshold for platelet aggregation by ADP in vitro was significantly lower in samples taken from the smokers at rest (1.4 +/- 0.9 mumol L(-1)) than in the non-smokers (3.5 +/- 2.5 mumol L(-1)), and the difference persisted both in the upright posture and after exercise. The level of platelet release of beta-thromboglobulin was, likewise, higher in the smokers in the upright posture. Neither standing up nor physical exercise had any significant influence on either of these two indices of platelet activity. The euglobulin clot lysis time was slightly longer in the smokers than in the non-smokers in all three experimental situations, but the differences were not significant. Inhibitor of tissue plasminogen activator was not materially different in the two groups (Table 2). The results indicate that smoking adds a further element of heightened platelet activity to that inherently present in hypertension.
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PMID:Smoking further increases platelet activity in patients with mild hypertension. 868 55

Healthy 19-year old males from the 95th percentile of mean arterial screening blood pressure were randomized to prolonged mental stress by receiving a letter informing of a high screening blood pressure (n = 13), or a neutral letter (n = 13). Blood platelet function in vivo was assessed by measurements of plasma concentrations of the platelet-specific protein beta-thromboglobulin, platelet counts, and mean platelet volumes before and during two laboratory stress tests (hand cold pressor test and arithmetic challenge). The cold pressor test caused a significant increase in beta-thromboglobulin concentrations in both groups, and significantly more in the uniformed group. Platelet count increased significantly in both groups during mental arithmetic with significantly higher counts in the uninformed group. Overall plasma beta-thromboglobulin responses were significantly larger in the uninformed group. This study demonstrates that laboratory stress is associated with blood platelet activation and that awareness of high blood pressure attenuates the platelet responses to such stress tests.
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PMID:Blood platelet responses to laboratory stress in young men. The effect of awareness of high blood pressure. 883 1

To assess platelet changes in pregnant women with chronic glomerulonephritis (CGN) and essential hypertension (EH) we estimated platelet lactic dehydrogenase activity (LDH), beta-thromboglobulin and thromboxane B2 (TxB2) plasma levels and ADP-stimulated platelet aggregability. Five groups of gravidae (26-40 weeks of gestation) were studied: with EH (n = 20), with CGN and hypertension (n = 31), with CGN without hypertension (n = 29), with late toxemia (n = 11), nonpregnant CGN women (n = 10) and healthy pregnant women (n = 20). Activation of platelet function was found in gravidae with CGN and EH. Platelet disorders were especially pronounced in pregnant women with CGN and with EH, but they were less pronounced than in control group with late toxemia. We believe that hypertension is more important stimulating factor for platelet activation than renal disease. We suggest that platelet disorders in outpatients are brought about by endothelium damage caused by elevated blood pressure.
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PMID:[Thrombocytic disorders in pregnant women with chronic glomerulonephritis and hypertension]. 902 46

It has been suggested that long term treatment with calcium antagonist drugs might inhibit platelet function and lead to an anti-atheromatous effect. However recent data have also suggested that such an effect might increase mortality due to an increased incidence of gastrointestinal bleeding. We identified 43 subjects from general practice with uncomplicated mild to moderate hypertension to compare the effects of the calcium antagonist isradipine with that of the beta-blocker atenolol on platelet function, plasma beta-thromboglobulin levels, fibrinolysis, and serum lipids in a randomised double-blind parallel group study. After careful evaluation to exclude concomitant aspirin use, only 24 subjects were eligible to enter the study. While isradipine and atenolol produced comparable and clinically significant falls in blood pressure (167 +/- 2/102 +/- 1 to 153 +/- 3/91 +/- 2 mm Hg, and 165 +/- 2/101 +/- 1 to 156 +/- 4/91 +/- 2 mm Hg, respectively), neither drug produced a detectable effect on ex vivo platelet aggregation, platelet retention, or thromboxane generation with adrenaline, collagen, adenosine-di-phosphate, or platelet activating factor. However a decrease in plasma beta-thromboglobulin levels was observed which reached statistical significance (P < 0.05) after 12 weeks treatment in the isradipine but not the atenolol group. A 39% reduction with isradipine compared with 34% following atenolol treatment. Euglobulin clot lysis time was not altered by either drug. Serum cholesterol concentrations were also unaltered by drug treatment. Therapeutic doses of the calcium antagonist isradipine may produce a minor indirect effect on platelet function after several weeks of treatment. However, this is of doubtful clinical importance and may simply reflect an effect of lowered blood pressure on platelet function.
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PMID:Pro-haemorrhagic effects of calcium antagonists: a comparison of isradipine and atenolol on ex vivo platelet function in hypertensive subjects. 946

Platelet-derived growth factor (PDGF) could play a role in both vascular hypertrophy and atherosclerotic disease associated with hypertension. To assess whether plasma PDGF level is increased in mild essential hypertension, we measured plasma PDGF concentration in 25 never-treated patients with uncomplicated mild essential hypertension and in 22 normotensive healthy subjects. To evaluate the contribution of platelets to plasma PDGF in the two groups, we also measured plasma beta-thromboglobulin (BTG). Measurement of PDGF was carried out through an enzyme-linked immunoadsorbent assay, which detects two PDGF dimers, namely PDGF-BB and PDGF-AB. Both plasma PDGF and BTG were higher in the hypertensive than in the normotensive subjects. The ratio of PDGF to BTG was similar in the two groups. Plasma PDGF was weakly correlated with plasma BTG in the normotensive subjects, whereas this relationship was lost in the hypertensive patients. Our results suggest that the increase in plasma PDGF (PDGF-AB + PDGF-BB) in never-treated essential hypertension is mainly due to platelet activation. The increased circulating level of PDGF could play a role in the vascular structural changes associated with hypertension.
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PMID:Increased plasma levels of platelet-derived growth factor (PDGF-BB + PDGF-AB) in patients with never-treated mild essential hypertension. 979 41

Increased inflammatory activity and platelet activation have been associated with an increased risk of cardiovascular (CV) events in epidemiological studies, but their prognostic importance in patients with stable angina pectoris is less well established. The Angina Prognosis Study in Stockholm (APSIS), comprised 809 patients (2766 patient years) with stable angina pectoris on double-blind treatment with verapamil or metoprolol. Plasma levels of fibrinogen and orosomucoid (an acute phase reactant), white blood cell counts (WBC), platelet counts and the urinary excretion of beta-thromboglobulin (reflecting platelet secretion), were related to the risk of CV death (n=36), non-fatal myocardial infarction (MI) (n=30) or revascularization (n=99) in a subgroup of 782 patients. Verapamil and metoprolol had only minor effects on the inflammatory variables. In multivariate Cox regression analyses (adjusted for previous MI, hypertension, diabetes mellitus and smoking), fibrinogen and WBC were independent predictors of CV death or non-fatal MI, as well as the risk of revascularization. Orosomucoid did not carry any independent information. Platelet counts and urinary beta-thromboglobulin were not significantly related to CV prognosis. The treatment given did not significantly influence the prognostic impact of either fibrinogen or WBC. Fibrinogen and WBC were independent predictors of CV death or non-fatal MI as well as disease progression leading to revascularization in patients with stable angina pectoris. As fibrinogen is also an acute-phase reactant, the present findings indicate that inflammatory activity is involved in disease progression in stable angina pectoris.
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PMID:Inflammatory and hemostatic markers in relation to cardiovascular prognosis in patients with stable angina pectoris. Results from the APSIS study. The Angina Prognosis Study in Stockholm. 1058 Jan 84

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

Ten cases of atherothrombotic brain infarction, 10 cases of cardioembolic brain infarction, 10 cases of lacunar brain infarction, 10 cases of transient ischemic attack (TIA) and 10 age-matched controls were studied. The cerebral blood flows in the cerebral cortex and cerebral white matter were significantly lower in the atherothrombotic, cardioembolic and lacunar infarction groups than in the TIA and control groups. The acetazolamide reactivity in the cerebral cortex was significantly lower in the atherothrombotic and lacunar infarction groups than in the cardioembolic, TIA and control groups. The rate of association of hypertension was significantly higher in the atherothrombotic, lacunar and TIA groups than in the cardioembolic and control groups. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were higher in the atherothrombotic, cardioembolic and lacunar groups than in the TIA and control groups. The present study suggests that the degree of thrombolysis and platelet activation is less in TIA than in cerebral infarction and that underlying cerebral arteriosclerosis is more severe in atherothrombotic and lacunar infarction than in cardioembolic infarction.
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PMID:Acetazolamide reactivity in atherothrombotic, cardioembolic and lacunar infarctions. 1075 Mar 58

The effect of quinapril and nifedipine on platelet aggregation, vascular endothelial function and coagulation system activity, was compared in a parallel-group, investigator-blind study carried out on patients with mild to moderate hypertension but no other diseases or receiving medication which might affect platelet function, vascular endothelium or coagulation. Forty patients (two groups of 20 patients each) and 20 control subjects were recruited. Patients were randomised to receive either quinapril or nifedipine retard and the dose escalated to control hypertension. Platelet aggregation studies were assessed serially and beta-thromboglobulin, angiotensin-converting enzyme (ACE), von Willebrand factor (vWF) coagulation factors VIIIc, XII and fibrinogen were measured at the beginning and end of the 12-week period. Blood pressure was adequately controlled in all patients in both groups. Platelet function was impaired in certain parameters (slope of the reaction with ADP and collagen and maximum aggregation with collagen) in the patient group compared to controls before treatment and this improved in patients on quinapril but not on nifedipine; likewise beta-thromboglobulin was higher in the patient group and fell significantly in the quinapril group but not those on nifedipine. Measurements of endothelial function and coagulation were normal before treatment and showed no alteration during the study, except in the expected fall in plasma ACE in the quinapril group. The results indicate that the ACE inhibitor, quinapril, has a beneficial effect on platelet function unlike the calcium channel blocker, nifedipine.
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PMID:A single (investigator)-blind randomised control trial comparing the effects of quinapril and nifedipine on platelet function in patients with mild to moderate hypertension. 1148 79


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