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

Plasma catecholamine concentration and platelet aggregation were studied in 22 patients with uncomplicated primary hypertension and 13 age-matched normotensive, healthy subjects at rest and in some during isometric handgrip exercise. The effect of norepinephrine (NE) infusion upon platelet aggregation was also examined. Plasma catecholamine concentration was slightly higher in the hypertensive than the normotensive group, but the difference was not significant. However, platelet aggregation to ADP was significantly greater in the hypertensive than the normotensive subjects. Exercise increased significantly both catecholamines and aggregation in both groups. Platelet aggregation was correlated with age (r = 0.62, P less than 0.01) and plasma NE (r = -0.34, P less than 0.05 for the total group of subjects). The infusion of NE increased significantly plasma NE and platelet aggregation and there was an inverse correlation between NE increase and threshold decrease (r = -0.69, P less than 0.05). Thus, plasma catecholamines and important determinants of platelet aggregation. However, in our study, uncomplicated primary hypertension was not associated with abnormal plasma catecholamine concentration. It is likely that the observed abnormal platelet aggregability to ADP represents a secondary phenomenon, possibly related to more advanced atherosclerotic vascular changes in hypertensive than normotensive subjects.
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PMID:Platelet aggregation in relationship to plasma catecholamines in patients with hypertension. 46 25

Platelet aggregability was measured using the screen filtration pressure (SFP) method in 50 elderly healthy people, 93 persons with essential hypertension, 166 patients with cerebral thrombosis at the recovery stage (more than two months after onset), and 74 patients with cerebral hemorrhage at the recovery stage. SFP by 3 muM ADP in the healthy persons, the hypertensive patients, and the patients in the recovery stages of hemorrhage and thrombosis were 148.7 +/- 53.5, 176.2 +/- 74.4, 189.8 +/- 58.3 and 206.3 +/- 58.9 mm Hg, respectively. The differences of the SFP between the Healthy and each of the diseased groups were statistically significant (P less than 0.01 to 0.05). Meanwhile, SFP of nine patients with cerebral thrombosis and 18 patients with hemorrhage was measured during their time course of disease from the onset to 180 days. SFP in the acute stage of thrombosis showed an increase and a gradual decrease during the time course, while SFP in the acute stage of hemorrhage showed the opposite -a decrease and a gradual increase. A statistically significant difference was observed between both groups within 30 days from onset (P less than 0.001). Screen filtration pressure in the acute stage of hemorrhage showed 95.2 +/- 17.7 mm Hg in nine survival cases and 194.0 +/- 96.2 mm Hg in nine deaths with ten days from the onset. The difference was statistically significant (P less than 0.001). Such results suggest a role of platelets in cerebral thrombosis and hemorrhage and a usefulness in differential diagnosis of both diseases.
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PMID:Platelet aggregability measured by screen filtration pressure method in cerebrovascular diseases. 96 Jan 62

Prazosin which is a selective alfa-1 blocking drug has a very good antihypertensive effect. Its hemorheological effects were studied in 20 patients with essential hypertension (I and II degree according to WHO classification). After 6 weeks of the therapy with prazosin, hematocrit and viscosity of the whole blood and plasma were significantly reduced, because of hemodilution, while aggregability of erythrocyte and "Tk" values were not significantly reduced. Platelet aggregation induced by collagen, ADP and adrenaline, showed a decrease after the treatment. Assuming the hemorheological effects not to be crucial in choosing an antihypertensive agent, we must not, however, neglect them, especially in patients with compromised hemorheological profile, and we should take advantage of the positive hemorheological effect of prazosin, particularly in a long antihypertensive treatment.
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PMID:[Hemorheologic changes in patients with essential hypertension treated with prazosin]. 134 59

Plasma humoral factors which modulate the transmembrane distribution of sodium and calcium have been identified in hypertensive patients and have been hypothesized to be involved in the etiology of essential hypertension. In cross-incubation experiments, we have found that plasma of hypertensive subjects elevated basal and stimulated intraplatelet calcium levels, while plasma of normal subjects has an opposite effect on platelets from hypertensives. Basal intraplatelet calcium in normal platelets was 108 +/- 5 nmol/L and rose to 142 +/- 3 nmol/L (P less than .001) after incubation in plasma from hypertensive patients. Platelets from hypertensive patients had basal calcium levels of 182 +/- 11 nmol/L which fell to 127 +/- 11 nmol/L (P less than .01) after incubation in normal plasma. Hypertensive plasma potentiated the rise in intraplatelet calcium in response to ADP and PAF. Hypertensive patients treated experimentally with plasmapheresis exhibited a disappearance of the plasma factor responsible for elevating intraplatelet calcium. These results indicate the presence of a plasma humoral factor in hypertensives which elevates intraplatelet calcium and sensitizes platelets to agonist stimuli.
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PMID:Humoral factor, intraplatelet calcium, and hypertension. 163 35

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

Plasma beta-thromboglobulin, initial (spontaneous) and total platelet aggregation, induced by adrenaline or ADP, were determined in 15 patients with essential hypertension before and after 1 week of diltiazem therapy. Diltiazem significantly decreased the spontaneous platelet aggregation in a therapeutic dose of 3 x 60 mg/day. This antiaggregatory effect is the further advantage of the antihypertensive therapy with diltiazem that may be of importance for the inhibition of atherosclerotic and thrombotic complications in essential hypertension.
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PMID:Diltiazem inhibits the spontaneous platelet aggregation in essential hypertension. 183 33

In various models of hypertension of genetic origin, a hypersensitivity of phospholipase C has been demonstrated to participate in the hyperreactivity of platelets toward a variety of vasoactive agents. Since this abnormality could not be observed in the absence of cell stimulation, it could not account for the increase in free Ca2+ which has been reported in resting platelets in primary hypertension. Likewise, in hypertensive subjects, platelets behave hyperactive when stimulated by ADP, although the stimulus has been demonstrated to be a poor activator of phospholipase C. In order to gain insight into the membrane alteration that could account for the cellular hyperactivity which characterizes hypertensive subjects, we investigated, in resting platelets, the kinetics of radioactive labeling of major membrane phospholipids. Isolated platelets were prepared from SHR (4w and 17w of age), SHR-SP, Dahl salt-resistant and salt-sensitive rats fed either a low or a high salt diet, DOCA-salt hypertensive rats and from the appropriate normotensive controls. Irrespective of the radioactive precursor used (32P-orthophosphate, 3H-glycerol, 3H-choline), the labeling of phosphatidylcholine (PC) was markedly (up to 20 fold) enhanced in SHR (whichever their age) and SHR-SP compared with WKY. This increase, specific of PC, could not be accounted for by differences either in the actual amount of PC or in the uptake of various labels, suggesting an increased PC turnover. Such an increase was also observed in platelets of Dahl hypertensive rats but not in those of DOCA-salt hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membrane abnormalities and cellular hyperreactivity in different models of hypertension]. 212 54

Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or ADP) were determined in twenty-eight normotensive subjects and thirty patients with untreated essential hypertension. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measurements were repeated in eighteen essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline- and ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on platelet aggregation. The results show that increased in vivo activation as well as increased platelet aggregation need not be restored to normal after effective decrease of blood pressure. The results suggest that a combination of drugs with an antihypertensive and antiplatelet (antiaggregating) effect (or use of a drug with both an antihypertensive and antiaggregating effect) can further decrease the development of severe complications of essential hypertension.
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PMID:Beta-thromboglobulin and platelet aggregation in essential hypertension and the influence of prazosin therapy. 214 48

1. Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or adenosine diphosphate [ADP]) were determined in 26 normotensive subjects and 26 patients with untreated essential hypertension. Groups of 18 essential hypertensive patients and 18 age- and sex-matched normotensives were compared. 2. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measures were repeated in 18 essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline-induced as well as ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on initial and total aggregability. 3. The results confirm increased platelet aggregation and in vivo platelet activation in patients with essential hypertension; however there is a discrepancy with previous reports about those results obtained after prazosin therapy. The results suggest that increased platelet aggregation and in vivo activation need not be restored to normal after effective antihypertensive therapy alone. They give reason for the combination of antihypertensive together with anti-aggregatory therapy in essential hypertension.
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PMID:The effect of prazosin therapy on platelet activation in essential hypertension. 215 Nov 84


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