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

The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.
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PMID:Platelet function during antihypertensive treatment with quinapril, a novel angiotensin converting enzyme inhibitor. 170 46

Platelet function was investigated in healthy volunteers and patients with essential hypertension by measurement of thresholds for ADP and adrenaline-induced aggregation and plasma concentrations of platelet factor 4 (PF-4) and beta-thromboglobulin (beta-TG) after administration of antihypertensive drugs. Fibrinolytic activity was investigated by the euglobulin clot lysis time (ECLT) and tissue plasminogen activator (t-PA) activity. Compared to normotensive controls, patients with essential hypertension showed increased aggregation as evidenced by a decrease in ADP thresholds for ex vivo platelet aggregation. ECLT was significantly prolonged and t-PA significantly lowered, indicating impaired fibrinolytic activity in mild hypertension. In different studies, we have shown that various antihypertensive drug regimens differ in their effects on platelet function and fibrinolytic activity when given to healthy volunteers or patients with mild-to-moderate essential hypertension. In normal volunteers, treatment with the calcium antagonists verapamil, nifedipine, and felodipine lowered plasma concentrations of PF-4 and beta-TG, indicating a reduced platelet activity in vivo. Fibrinolytic activity was not influenced by calcium antagonist treatment in the normal volunteers. Interestingly, however, t-PA increased significantly in the hypertensive group. When compared to placebo or beta 1-selective blockers, propranolol, a non-selective beta-adrenergic blocker without partial agonist activity, reduced ADP and adrenaline threshold values for ex vivo platelet aggregation in hypertensive subjects and impaired fibrinolytic activity in the normal volunteers as well as in the hypertensive groups by increasing ECLT and reducing t-PA. Hypothetically, the effects of antihypertensive drugs on platelet function and fibrinolytic activity could be of importance for their proposed actions on cardiovascular morbidity and mortality.
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PMID:Platelet function and fibrinolytic activity in hypertension: differential effects of calcium antagonists and beta-adrenergic receptor blockers. 172 42

The influence of the sympathetic nervous system on platelet functions in vivo is still controversial. The aims of our study were to compare the response to various sympathetic stimuli in normal subjects and in patients with essential hypertension (HT) or peripheral vascular disease (PVD) and to evaluate any correlations among plasma levels of catecholamines, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4). In basal conditions beta-TG and PF4 values in the HT patients were higher than those observed in the controls of the same age but lower than those of the PVD patients. Although the different sympathetic stimuli (90 degrees tilting, handgrip, treadmill test, bicycle test) caused a significant increase of the plasma epinephrine (E) and norepinephrine (NE) levels, they did not modify the beta-TG and PF4 levels in any of the groups studied. The platelet activation indices, therefore, regardless of the basal values, do not seem to be influenced by sympathetic stimulation.
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PMID:Beta-TG and plasma catecholamines levels after sympathetic stimuli in hypertensives and patients with peripheral vascular disease. 214 20

To clarify the mechanism for cold-related thrombosis, we evaluated responses of blood pressure, platelet function, and sympathetic nervous activity after cold exposure in ten healthy male volunteers (33 +/- 2 years old). Mean blood pressure, beta-thromboglobulin, platelet factor 4, and plasma noradrenaline were increased after cold exposure associated with significant falls in skin, oral, and urine temperature. The increase in plasma noradrenaline significantly correlated with the change in platelet aggregation (3 microM ADP: r = 0.73, P less than .02, 3.0 micrograms/mL epinephrine: r = 0.65, P less than .05), and with mean blood pressure in the warn environment (r = 0.76, P less than .02). These results suggest that the cold-related increase in sympathetic nervous activity may contribute to enhancement of platelet function. This provides a possible explanation for the risk of thrombosis in cold weather in essential hypertension.
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PMID:Acute effects of exposure to cold on blood pressure, platelet function and sympathetic nervous activity in humans. 252 81

Beta-thromboglobulin (BTG) and platelet factor 4 (PF4), platelet alpha-granule specific proteins, and serotonin (5-HT) which is stored in dense granules are released when platelets are activated. To investigate in vivo platelet activation in uncomplicated essential hypertension, platelet 5-HT and PF4 contents, plasma BTG and PF4 concentrations, as well as urinary BTG levels were assessed in normotensive and hypertensive subjects. Plasma BTG and PF4 concentrations and urinary BTG levels were comparable in both groups. Mean platelet 5-HT content was significantly decreased in hypertensive subjects without modification of the intraplatelet PF4 content. These data suggest first of all that the decrease in platelet 5-HT content is due mainly to the inhibition of platelet 5-HT uptake previously described, and second of all that no significant in vivo platelet activation occurs in essential hypertensive subjects devoid of cardiovascular complications.
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PMID:Study of in vivo platelet activation in uncomplicated essential hypertension. 294 31

In order to investigate whether an altered "in vivo" platelet serotonin release contributes to the low platelet serotonin content observed in essential hypertensive patients, we have measured plasma concentrations of beta-thromboglobulin and platelet factor 4, urinary beta-thromboglobulin concentrations and platelet serotonin and platelet factor 4 contents in 11 untreated essential hypertensive patients (WHO Stage I) and in 12 age-matched normotensive controls. Beta-thromboglobulin and platelet factor 4 are specific platelet proteins localized in the alpha-granules which are released during in vivo platelet activation. Plasma and urinary concentrations of these alpha granule proteins determined by radioimmunoassay were found to be similar in hypertensive and normotensive subjects. The low platelet serotonin content determined by high pressure liquid chromatography from platelet rich plasma in hypertensive patients (0.282 +/- 0.008 vs 0.348 +/- 0.019 nmol/10(8) platelets, p less than 0.01) was not associated with a decrease in platelet 4 content (1.36 +/- 0.07 vs 1.36 +/- 0.10 microgram/10(8) platelets). This study shows that platelet alpha-granule content is unaltered in uncomplicated essential hypertension and suggests that the low platelet serotonin content in hypertensives is mainly due to the inhibition of platelet serotonin uptake.
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PMID:[In vivo platelet activation in mild arterial hypertension]. 295 30

The ratio of the plasma level of beta-thromboglobulin (beta-TG) to platelet factor 4 (PF-4) which is regarded as a most reliable indicator of platelet activation in vivo, was followed in 52 subjects at various stages of essential hypertension according to the WHO classification. These comprised 30 cases at stage I, 19 cases at stage II and three cases at stage III, and 20 age-matched normotensive control subjects. The observed beta-TG:PF-4 ratio in the hypertensive patients was 4.59 +/- 0.20, which was significantly higher than the value of 3.13 +/- 0.19 recorded in the normotensive control subjects. According to the WHO classification, beta-TG:PF-4 ratios in hypertensive patients at stages I, II and III were 3.93 +/- 0.19, 5.31 +/- 0.35 and 6.56 +/- 0.12, respectively. The beta-TG:PF-4 ratio revealed a tendency of platelet activation to increase with advanced progress of hypertensive vascular lesions. These results suggest that the abnormal platelet function observed in patients with essential hypertension plays an important role in the development of hypertensive vascular complications.
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PMID:Plasma beta-thromboglobulin to platelet factor 4 ratios as indices of vascular complications in essential hypertension. 296 97

Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.
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PMID:Diltiazem in hypertensive patients with type II diabetes mellitus. 317 28

Platelet catecholamine content may reflect integrated plasma catecholamine concentrations over time. The present study aimed at examining sympathetic nervous system (SNS) involvement in essential hypertension by assessing platelet noradrenaline (NA) and typically beta-adrenoreceptor mediated responses to adrenaline (A) infusion as indices of sympathetic tone. Healthy white men were recruited by public advertising and screening (mean +/- SD): Hypertensives (n = 13, sitting blood pressure [BP] 153 +/- 13/106 +/- 7 mmHg, age 34 +/- 5 years, weight 83 +/- 10 kg) were compared to normotensives (n = 13, sitting BP 114 +/- 9/75 +/- 9 mmHg, age 30 +/- 6 years [n.s.], weight 82 +/- 9 kg [n.s.]). Loss of platelet granular contents (including NA) prior to analysis was minimized by studying young subjects (age range 20-40 years, minimal atherosclerosis), using arterial blood sampling, and processing blood immediately. These procedures resulted in plasma beta-thromboglobulin and platelet factor 4 levels which were not significantly different between groups. Sympathetic activation resulting from stress was minimized by not labelling subjects as either hypertensive or normotensive. Mean arterial platelet NA content was significantly higher in hypertensives (64 +/- 31 pg/mg of platelet weight) compared to normotensives (43 +/- 20 pg/mg, p < 0.05) both at baseline and following 35% expansion of the circulating platelet pool by A infusion (p < 0.05) and correlated with arterial NA in the hypertensives (r = 0.79, p < 0.002) but not in the normotensives (r = 0.04, n.s.). Similar increases in platelet and plasma A during infusion in both groups suggest unchanged platelet uptake capacity and plasma clearance in the hypertensive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic nervous system involvement in essential hypertension: increased platelet noradrenaline coincides with decreased beta-adrenoreceptor responsiveness. 806 4

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


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