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)

We followed 19 men and 19 women with asymptomatic carotid stenosis up to 30 months to determine whether hematologic or lipid abnormalities could identify those individuals developing progressing carotid atherosclerosis (defined as an increase in mean percent stenosis greater than or equal to 19% or an increase in a single region of greater than or equal to 23%) on B-mode carotid ultrasonography performed at 2- to 6-month intervals. Our patients demonstrated increased beta-thromboglobulin, platelet factor 4, and fibrinogen compared with age-matched controls. Eight patients developed progression of carotid stenosis, and this group had higher baseline low-density lipoprotein (LDL) and fibrinogen than the 30 nonprogressing patients. Multiple regression analyses of age, sex, smoking, coronary artery disease, peripheral vascular disease, diabetes, hypertension, and baseline high-density lipoprotein (HDL), HDL2, HDL3, LDL, beta-thromboglobulin, platelet factor 4, and fibrinogen identified coronary artery disease and elevated LDL and fibrinogen as the only independent variables significantly associated with the progressing group. We conclude that, in patients with carotid atherosclerosis, a combination of coronary artery disease and elevated LDL and fibrinogen will predict with 88% accuracy whether the patient will have progressing carotid stenosis.
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PMID:Prediction of carotid stenosis progression by lipid and hematologic measurements. 218 78

Endothelial injury and platelet activation may be involved in the pathogenesis of hypertensive vascular disease. The aim of this study was to evaluate the change in endothelial cell and platelet activation plasma markers after an acute physiological increase in blood pressure. Plasma renin activity (PRA), serum angiotensin-converting enzyme (ACE), plasma factor VIIIR:Ag, and plasma beta-thromboglobulin (BTG) were determined before and after handgrip in subjects with borderline (n = 8) and established (n = 11) hypertension and in age-matched normal volunteers (n = 10). A significant mean increase in ACE, factor VIIIR:Ag, and BTG was observed after handgrip in all groups of subjects. A greater response in BTG changes was found in hypertensive subjects when compared with normal subjects. No correlations were found between the blood pressure response after handgrip and the handgrip-induced changes in plasma markers of endothelial cells and platelet activation. Changes in endothelial cells and platelet activity occurring after handgrip did not appear to depend on the associated blood pressure elevations.
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PMID:Plasma markers of endothelial cells and platelet activation following handgrip in normals and hypertensive patients. 283 26

Compared with normotensive pregnant women (n = 13), patients with severe pre-eclampsia (n = 13) had increased arterial plasma adrenaline (P < 0.001), peripheral venous adrenaline (P < 0.01), arterio-venous differences of adrenaline (P < 0.001) and venous concentration of the platelet release product beta-thromboglobulin (P < 0.001). In the pre-eclamptic group, arterial adrenaline correlated with mean blood pressure (r = 0.90, P < 0.001), heart rate (r = 0.78, P < 0.01) and beta-thromboglobulin (r = 0.82, P < 0.001), while in the normotensives adrenaline correlated only with beta-thromboglobulin (r = 0.76, P < 0.01). According to these results, sympathetic adrenal tone is increased in pre-eclampsia and may play a role in the pathogenesis of high blood pressure and platelet activation in this disease.
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PMID:Increased arterial adrenaline is highly correlated to blood pressure and in vivo platelet function in pre-eclampsia. 285 91

Ketanserin is a new strong antiserotoninergic drug that, unlike the previous ones, is selective for 5-hydroxytryptamine receptors. This drug has been employed successfully in the treatment of arterial hypertension and of some peripheral vascular diseases. The authors are carrying out a trial on medium term treatment with ketanserin (K) or propranolol (P) in comparison with placebo, to evaluate their effects on blood pressure, haemocoagulative parameters and peripheral circulation. The trial is a double-blind cross-over random trial on subjects with mild or moderate hypertension. Until now 13 patients have ended the study; six of them are suffering from arteriosclerosis obliterans of the lower limbs at 1st or 2nd stage according to Fontaine. Both propranolol and ketanserin significantly reduced the blood pressure, although the decrease in systolic blood pressure was more evident after propranolol. Heart rate diminished significantly only after propranolol administration. The noninvasive, intermittent (every 30 min) monitoring of blood pressure showed a significant 24-hour reduction of blood pressure after administration of propranolol or ketanserin without significant changes of circadian behaviour of the blood pressure. After administration of ketanserin a slight improvement in peripheral circulation was demonstrated, evaluated by using strain-gauge plethysmography. As regards the results obtained for platelet function and other haemocoagulative parameters examined, adenosine diphosphate-induced platelet aggregation, adenosine diphosphate slope, collagen lag period, antithrombin III biological activity, and serum fibrinogen did not show noticeable modifications after treatment, while beta-thromboglobulin levels decreased slightly after ketanserin administration.
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PMID:Effects of ketanserin on blood pressure, peripheral circulation and haemocoagulative parameters in essential hypertensives with or without arteriosclerosis obliterans of the lower limbs. 294 85

50 year old men with moderate, essential hypertension (n = 39) were compared to normotensive males of similar age (n = 31). The hypertensive men were heavier (10 kg in average, p less than 0.01), and had a higher pulse rate (5 beats per minute (p less than 0.05). Plasma beta-thromboglobulin, a marker of platelet release reaction, was 49% higher in the hypertensive group (p less than 0.01). Total cholesterol, LDL + VLDL cholesterol and serum triglycerides were not significantly different between the groups. In the hypertensive group, plasma beta-thromboglobulin concentration correlated significantly with total cholesterol (r = 0.47, p less than 0.01) as well as with LDL + VLDL cholesterol (r = 0.50, p less than 0.01). In the normotensive group no such correlation was found. The results suggest activation of platelets in hypertension, and suggest that in hypertension, even a normal cholesterol concentration may influence platelet function.
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PMID:Blood platelet release correlates with serum lipids in 50 year old men with essential hypertension. 295 73

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.
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PMID:Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension. 295 74

Blood platelet function was evaluated in 10 men, all 50 years old, with untreated, mild hypertension. Each patient was examined four times: At the beginning of the study, after 5 weeks on placebo treatment, after the following 5 weeks on propranolol 160 mg daily, and finally after a second period of 5 weeks on placebo. At baseline the plasma level of the platelet release product beta-thromboglobulin (BTG) was 41.6 (30.5-57.0) micrograms/l (median and 95% confidence interval). During the first placebo period BTG was normalized to 21.0 (14.1-25.9) micrograms/l. While systolic blood pressure and heart rate fell during beta-adrenergic receptor blockade, BTG remained unchanged throughout the rest of the observation periods. Platelet size increased significantly during treatment with beta-blocker. The present study indicates that the normalization of elevated platelet function which previously has been reported to occur during anti-hypertensive drug therapy, may be explained by patient adaptation to the blood sampling procedure.
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PMID:Does increased platelet release normalize during anti-hypertensive treatment? 296 2

During low-dose adrenaline infusion, platelet count, platelet size, plasma beta-thromboglobulin (BTG) and forearm vascular resistance (FVR) were measured in twelve 40-year-old men with mild, untreated hypertension. The average platelet count increased from 195 to 226 X 10(9)/l (P less than 0.001), platelet size from 7.31 to 7.53 X 10(-15)/l (P less than 0.01), BTG from 0.61 to 1.08 nmol/l (P less than 0.02) and FVR decreased from 97 to 58 (arbitrary units; P less than 0.001) during the infusion. The change in platelet count reflects splenic release of platelets, the change in plasma BTG reflects platelet release reaction, while the reduced FVR reflects vascular smooth muscle cell relaxation. In 11 normotensive men aged 40 years, platelet count increased from 187 to 201 X 10 g/l (P less than 0.01) during an equal low-dose adrenaline infusion. This increase in platelet count is significantly less than in the hypertensive group (P less than 0.01). There was statistically no significant change in platelet size, BTG or FVR in the normotensive group. Arterial adrenaline rose from 0.5 to 2.5 nmol/l in the hypertensive and from 0.5 to 2.4 nmol/l in the normotensive group. A third group of 12 normotensive men received saline infusion: neither platelet parameters nor FVR changed in this group. Thus, a small and equal dose of adrenaline elicited a greater increase in platelet count, an enhanced platelet release reaction and a more pronounced forearm vasodilation in hypertensive than in normotensive subjects.
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PMID:Increased platelet and vascular smooth muscle reactivity to low-dose adrenaline infusion in mild essential hypertension. 296 93

In arterial hypertension, hyperviscosity with hemorheological disturbances and platelet dysfunction may play a role in the prognosis and complications of the disease. We studied the effects of Nicardipine (NIC) on these blood disturbances in a group of 21 untreated patients with essential hypertension, aged 25 to 70 years (SBP/DBP = 185 +/- 28/105 +/- 17 mmHg). During one hour before and 4 hours after the IV injection of single doses of 5, 7.5 or 10 mg NIC over 5 min, blood pressure was recorded automatically (Dinamap). Hemorheological variables and platelet function were studied before and 30 min, 3 h and 24 hours after the injection. NIC lowered blood pressure and increased heart rate significantly (At 5 min, SBP = -24 mmHg; DBP = -18 mmHg; HR = +22 b/min). These effects were dose-dependent with rapid onset and short duration (less than 2 hrs). NIC decreased plasma viscosity from 1.36 +/- 0.08 to 1.30 +/- 0.07 Cst; p less than 0.01, whole blood viscosity from 22.4 +/- 2.8 to 20.7 +/- 1.5 mPas; p less than 0.05 for gamma = 0.512 s-1, and erythrocyte filterability with the Ca++ ionophore A 23187 from 16.3 +/- 3.8 to 13.5 +/- 3.1; p less than 0.01. Platelet aggregation with ADP was unchanged, but aggregation with A 23187 decreased from 46.9 +/- 21.2 to 31.3 +/- 25.6; p less than 0.05, as well as plasma levels of beta-thromboglobulin (71.2 +/- 29.8 to 55.4 +/- 24.3 ng/ml; p less than 0.02) and platelet generated malonaldehyde (7.2 +/- 1.8 to 6.7 +/- 1.4 nM/10(9) platelets; NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of intravenous nicardipine on blood pressure, hemorheology platelet function in arterial hypertension. Dose-effect relations]. 311 84

Platelet activation was assessed in hospitalized third-trimester patients with preeclampsia (n = 11) or chronic hypertension with superimposed preeclampsia (n = 11) and in healthy outpatient pregnant controls (n = 10) by measuring plasma beta-thromboglobulin, platelet factor 4, the platelet aggregate ratio, and the amount of collagen required to produce half-maximal aggregation velocity (Kd). Only plasma beta-thromboglobulin levels differed significantly between patients with preeclampsia (50.1 +/- 37.9; p less than 0.05) or chronic hypertension with superimposed preeclampsia (47.6 +/- 16.3; p less than 0.01) and the control subjects (22.5 +/- 11.3). beta-Thromboglobulin values in patients with preeclampsia, but not chronic hypertension with superimposed preeclampsia, correlated directly with 24-hour urinary protein loss (r = 0.93, p less than 0.001) and serum creatinine levels (r = 0.62, p less than 0.05) and inversely with creatinine clearance (r = 0.60, p = 0.05). We conclude that (1) beta-thromboglobulin is elevated in patients with preeclampsia or chronic hypertension with superimposed preeclampsia, (2) the normal platelet aggregate ratio and the Kd indicate that the increase in beta-thromboglobulin is not due to an intrinsic change in platelet responsiveness, and (3) the elevation of beta-thromboglobulin in patients with either preeclampsia or chronic hypertension with superimposed preeclampsia appears to be secondary to platelet consumption in the microvasculature, although in patients with preeclampsia altered renal function may be contributory.
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PMID:Platelet activation in preeclampsia. 315


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