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

Platelet aggregability was measured using platelet rich plasma (PRP) collected from 197 clinical cases including 52 healthy volunteers. In 31 patients of acute stage of thrombosis (within 2 weeks from the onset), a significant enhancement of platelet aggregation measured 5 min after an addition of 3 and 10 muM ADP or 0.1 and 1 mug/ml of adrenaline to PRP (p less than 0.05, compared to the healthy group). Also a significant enhancement of secondary aggregation induced by adrenaline was observed (p less than 0.05). The enhancement was especially marked in the response induced by adrenaline. Such an enhancement was not observed in patients in the recovery stage of thrombosis, hypertension, angina pectoris and other miscellaneous diseases. There was no difference in the parameters related to the velocity of aggregation or intensity of primary aggregation between the diseased and the healthy group. In response induced by collagen (bovine achilles tendon, 0.3 and 1 mg/ml) any difference in the aggregation curve was not observed between the diseased and the healthy group. Such findings suggest a presence of an enhancement of ADP-release mechanism of platelets in acute thrombosis. Aslo a significance of adrenaline-induced platelet aggregation was proposed to detect platelet functions for analysis of mechanism of thromboembolic disorders.
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PMID:Hyperaggregability of platelets in thromboembolic disorders. 24 93

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

In order to understand the pathogenesis of intracranial hypertension, the intracranial pressure (ICP) has usually been studied with the concept of volumetric pressure. In other words, the ICP is held to derive from the volume of the intracranial elements (e.g., brain, blood and cerebrospinal fluid). In this paper, the authors propose a new concept of the so-called driving pressure and apply it to both clinical and experimental studies. The driving pressure (DP) consists of the combined pressure continuously exerted on the ICP by the arterial pressure (ADP) and venous pressure (VP) systems.
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PMID:The analysis of the intracranial pressure by the concept of the driving pressure from the vascular system. 64 47

In order to understand the pathogenesis of increased intracranial pressure, the concept of the driving pressure (DP) from the intracranial vascular system was proposed. The DP consists of the transmission of atrial pressure (ADP) and venous pressure (vp). It is well known that when the animals died, the intracranial pressure decreased to the atmospheric pressure. This means that the DP is important in maintaining the static pressure of the cerebrospinal fluid. The theoretical equation of the intracranial pressure was expressed as follows.ICP=ADP+VP (1) ADP is expressed as (2). ADP=eta (BP-VP) (2) The pressure transmission rat (eta) was calculated as the ratio of the CSF pressure to the systemic arterial blood pressure in the experimental and clinical cases. In the normal CSF pressure, eta was very small (2.0 X 10(-2)), while in the severe intracranial hypertension, eta approached to 1. The concept of the driving pressure was useful to analyze the static intracranial pressure and the pulse pressure.
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PMID:[Intracranial pressure--volumetric pressure and driving pressure]. 103 40

Biphasic collagen-induced platelet aggregation, resembling that induced by epinephrine, was noted in platelet-rich plasma (PRP) of 11 stroke and 1 coronary disease patients. Similar pattern of aggregation was not observed in normal PRP. The occurrence of the biphasic collagen aggregation does not appear to relate to platelet count, smoking habit, medication, or other abnormalities such as hypertension, diabetes, and elevated serum lipid levels. However, platelets of these patients were very sensitive to aggregating agents including epinephrine and adenosine diphosphate. The concentration of collagen that elicited biphasic aggregation in these platelets was too weak to aggregate platelets of normal subjects. We believe that the release threshold of these platelets is reduced to such an extent that minute amounts of collagen, which would be insufficient to induce release from normal platelets, are capable of inducing release from these platelets. Both phases of collagen induced aggregation are probably resulted from the activation of the release mechanism.
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PMID:Characterization and significance of collagen induced biphasic aggregation of human platelets. 119 59

The relationship between blood pressure and platelet basal cytoplasmic calcium concentration ([Ca2+]i) and platelet sensitivity to aggregating agents in hypertension has been investigated in hypertensive patients and normotensive subjects. Ten severely hypertensive patients whose blood pressures were poorly controlled with metoprolol, were given calcium antagonist (either nifedipine or felodipine) as a second line agent. Venous blood samples were collected at each treatment phase for measurement, in whole blood, of platelet aggregation in response to ADP and collagen, and of basal [Ca2+]i using fura-2. Control of blood pressure by the combination of metroprolol and a calcium antagonist induced a significant decrease in median [Ca2+]i from 116 (76-181) to 73 (60-83) nM, which was similar to the median value of 70 (61-80) nM obtained in 14 normotensive subjects. Overall [Ca2+]i correlated with mean blood pressure (r = 0.51). Treatment of hypertension with calcium antagonist did not change the response of platelets to collagen or ADP. The results confirm that effective treatment of hypertension significantly reduced basal [Ca2+]i in platelets but raise doubts whether elevated basal [Ca2+]i is necessarily the sole mechanism by which the sensitivity of platelets to aggregatory agents is increased in hypertension.
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PMID:Treatment of hypertension induces a fall in platelet basal cytoplasmic calcium concentration without influencing platelet aggregation. 128 83

Little is known about the effect of low dose, enteric-coated aspirin on human blood platelet function. This study was conducted to evaluate the acute effects of a single daily dose of commercially available enteric-coated aspirin on platelet biochemistry, physiology and function. Blood for these studies was obtained from drug-free volunteer donors prior to ingestion of aspirin or following ingestion, either before breakfast or following lunch. Response of platelets to the action of weak agonists was evaluated. In addition, ability of platelets to convert radiolabeled arachidonic acid to thromboxane was monitored. Results of our studies show that a single daily dose of 50 mg of aspirin taken either before breakfast or after lunch effectively prevented the secondary wave aggregation response, as well as secretion of dense body contents when stimulated by agonists such as epinephrine and ADP. Aspirin ingestion caused a dose-dependent inhibition of platelet cyclooxygenase activity as evidenced by the extent of arachidonic acid converted to thromboxane by platelets exposed to aspirin for different time periods. Based on these observations, it is suggested that low dose aspirin may be very useful and desirable to restrain platelet activity in clinical situations in which increased thromboxane formation may initiate vascular hypertension and platelet hyperactivity.
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PMID:Influence of low dose enteric-coated aspirin on platelet function. 130 83

The present study investigated whether reduced adenylate cyclase activity and an increase in inhibitory guanine nucleotide binding proteins (Gi alpha), which have been observed in the failing human heart, already occur in myocardial hypertrophy before the stage of heart failure. In membranes of hypertrophic hearts from rats with different forms of experimentally induced hypertension without heart failure (one-kidney, one clip rats, deoxycorticosterone-treated rats, and rats with reduced renal mass), basal as well as isoprenaline-, 5'-guanylylimidodiphosphate-, and forskolin-stimulated adenylate cyclase activity was reduced. The activity of the catalyst was depressed in deoxycorticosterone but unchanged in one-kidney, one clip and reduced renal mass compared with controls. The number of beta-adrenergic receptors was similar in all groups. Radioimmunological quantification of Gi alpha proteins revealed an increase by 73% in one-kidney, one clip, 67% in reduced renal mass, but only 20% in deoxycorticosterone compared with sham-operated, age-matched control rats. The increase of Gi alpha was accompanied by smaller changes of pertussis toxin-induced [32P]ADP-ribosylation of a 40-kd membrane protein. It is concluded that Gi alpha contributes to the reduced adenylate cyclase activity in cardiac hypertrophy in one-kidney, one clip and reduced renal mass and to a smaller extent in deoxycorticosterone. It is suggested that an enhanced expression of Gi alpha could occur not only in severe heart failure but also in cardiac hypertrophy and could, therefore, contribute to myocardial depression and progression of disease in heart failure. In addition, Gi alpha might represent an important regulatory mechanism for cardiac adenylate cyclase activity and thus, might play an important role in various cardiac diseases.
Hypertension 1992 Jul
PMID:Desensitization of adenylate cyclase and increase of Gi alpha in cardiac hypertrophy due to acquired hypertension. 131 58

Hypercholesterolemia and hypertension are two of the major risk factors associated with increased atherosclerotic vascular disease. An abnormal platelet function is one of the mechanisms proposed to participate in atherogenesis. This study was undertaken to find out whether hypercholesterolemia in hypertensive patients can change platelet lipid composition and reactivity. Twenty-nine untreated hypertensive patients were distributed into 3 age, body mass index and blood pressure-matched groups according to their plasma cholesterol levels (normal, borderline or elevated, group NC, BC and HC respectively). Their platelet lipid composition, cytosolic Ca2+ concentration, cyclic AMP content and aggregating response to ADP and collagen were determined. Platelet from group HC patients were characterized by reduced cyclic AMP content (evaluated in the presence and absence of a platelet phosphodiesterase inhibitor) and aggregating responses to ADP and collagen, increased palmitic acid content and decreased arachidonic, eicosapentaenoic and docosatetraenoic and pentaenoic acid content, resulting in a lowered polyunsaturated to saturated fatty acid ratio (P less than 0.001). In contrast, platelet cytosolic Ca2+ concentration, DPH steady-state anisotropy and cholesterol to phospholipid molar ratio were not significantly changed. This indicates that hypercholesterolemia is accompanied in hypertensive patients by marked changes in platelet fatty acid composition, cyclic AMP content and response to aggregating agents. These changes, which clearly differ from those induced by in vitro cholesterol loading, could reflect not only the balance between LDL and HDL stimulation but also an adaptation to hemodynamic perturbations.
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PMID:Biochemical and functional alterations associated with hypercholesterolemia in platelets from hypertensive patients. 132 32

The effect of a four weeks oral treatment with 100 mg isosorbide dinitrate (ISDN) daily on platelet function was evaluated in 40 patients (aged 40-65 years) with proven coronary artery disease. Isosorbide dinitrate decreased platelet reactivity to ADP (p less than 0.001), increased platelet sensitivity to PGI2 (p less than 0.01) while the production of TXB2 from exogenous arachidonic acid substrate and from endogenous substrate were both significantly reduced. Circulating platelet aggregates as measured by the Wu-test were markedly reduced (p less than 0.001) but there was little change in the plasma concentration of the platelet proteins beta-thromboglobulin and platelet factor 4. Overall, platelet activation correlated with smoking, hypertension and a family history of coronary artery disease. The reduced platelet activation seen during treatment with isosorbide dinitrate may contribute to the therapeutic benefit seen with this drug in patients with coronary artery disease.
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PMID:Modification of platelet function by isosorbide dinitrate in patients with coronary artery disease. 138 8


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