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

A double-blind study was established to evaluate the platelet aggregation inhibiting effect of ticlopidine on the course of ocular vein occlusions. 35 patients with recent central retinal vein occlusions and 54 patients with retinal branch vein occlusions were treated for 6 months. Various ophthalmological and clinical-chemical parameters, including fluorescence angiography, were assessed. Compared with placebo therapy a significant improvement in visual acuity was observed with ticlopidine for branch vein occlusions; the same trend was seen for the central retinal vein occlusions. Increased ADP-induced platelet aggregation was frequently found: in 72% of the central retinal vein occlusions and 70% of the branch vein occlusions. For the Wu and Hoak test, these numbers were respectively 74% and 67%. Hypertension was seen in 55% of all occlusions, hyperlipaemia in 33%, and diabetes in 29%. The effect of ticlopidine was most pronounced in patients with increased platelet aggregation and least obvious in hyperlipaemia. Hypertension and diabetes did not apparently influence Ticlopidine's effects. It is concluded that the platelet aggregation inhibitor ticlopidine is effective in the treatment of recent ocular vein occlusions.
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PMID:The influence of ticlopidine on the natural course of retinal vein occlusion. 638 48

The aggregation properties of washed SHRSP platelets were investigated in comparison with normotensive WKY platelets at prehypertensive (4 weeks), early hypertensive (11 weeks) and late hypertensive (17 weeks) ages in the absence of plasma factors. The number of platelets in SHRSP was markedly lower with the development of hypertension than that in WKY. The thrombin- and collagen-induced aggregation was markedly reduced in the platelets from 11 and 17 week old SHRSP compared with that of age-matched WKY, whereas the degree of platelet aggregation in 4 week old SHRSP showed a tendency to be even greater than that in WKY. The changes in blood pressure and platelet aggregability were correlated inversely. ADP did not induce aggregation in the same system used for thrombin and collagen stimulation but in another system it aggregated washed rat platelets. Aggregation responses to ADP and ionophore A23187 were also significantly lower in 14 week old SHRSP platelets than age-matched WKY platelets. Together with other evidence, these results suggest that defective Ca2+ function, rather than the presence of exhausted platelets, is responsible for hypoaggregability in SHRSP platelets.
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PMID:Hypoaggregability of washed platelets from stroke-prone spontaneously hypertensive rats (SHRSP). 642 Sep 47

Three different methods of blood collection from rats are studied and compared, namely decapitation, catheterization of the carotid artery and puncture of the heart left ventricle. The latter method is preferable in studies of platelet aggregation. The method for isolation of washed platelets from rat blood is described in detail. The platelets stored for several hours at 20 degrees C did not lose the ability for aggregating under exposure to low concentrations of ADP. The curves of aggregation of washed and plasma platelets are provided. To study the rate of aggregation, a model is offered based on the approximation of the aggregation curves by the exponential A = A0exp (-alpha t). Such an approach made it possible to treat the data objectively and to reveal the features of platelet functional activity, particularly in arterial hypertension.
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PMID:[Method for collecting rat thrombocytes and determining their aggregation]. 646 16

Platelet aggregation in the post-acute phase of 48 patients with cerebral thrombosis was measured to see if any specific type of cerebral infarction is associated with enhanced platelet aggregation. All patients were examined with cerebral angiography and computed tomography (CT). Stenotic lesions in major cranial arteries were analyzed by measuring the apparent diameter. Severe stenosis was defined as 75 per cent constriction or more. Enhanced aggregation of platelets (secondary aggregation at 1 microM ADP or less) was present in 5 of 25 patients (20%) who had severe vessel stenosis or occlusion. CT examination frequently revealed both cortical and deep involvement. On the other hand, 13 of 23 patients (57%) with less stenotic lesions showed enhanced aggregation and that was statistically significant (p less than 0.05). Many patients of this group had persistent hypertension and small deep infarctions. Platelet aggregation was also measured in 20 hypertensive control subjects without stroke. Four of them (20%) showed enhanced aggregation. These findings suggest that a combination of enhanced platelet aggregation and hypertension increases the risk of small deep infarctions accompanied by mild stenotic changes of the major cranial arteries.
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PMID:Platelet aggregability in cerebral thrombosis--analyzed for vessel stenosis. 665 4

Hypertensive disease is known to increase the risks in connection with acute changes in blood pressure due to the presence of pronounced structural as well as functional changes in the cardiovascular system. In the present study the metabolic consequences of fixed haemorrhagic hypotension [mean arterial pressure (MAP) 70 and 45 mmHg] were studied in spontaneously hypertensive (SHR) and in normotensive rats (WKY). Blood gases and acid-base balance, blood glucose, liver (ATP, glucose, lactate) and brain (ATP, ADP, AMP, CP, glucose, lactate) metabolites were determined in unbled animals and after 35 min hypotension in bled animals. In the liver haemorrhage to MAP 70 mmHg resulted in a 70% reduction of the ATP content in SHR while that in WKY remained unchanged. At MAP 45 mmHg reduced liver ATP levels (35% reduction) were observed in WKY as well. In the brain metabolic changes indicative of tissue ischaemia (reduced CP, increased AMP and lactate, decreased energy charge potential) were present only in SHR at MAP 45 mmHg. The more pronounced metabolic disturbances in SHR than in WKY indicate that blood loss is more deleterious for the hypertensive individual.
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PMID:Effects of haemorrhagic hypotension on brain and liver metabolism in normotensive (WKY) and spontaneously hypertensive rats (SHR). 668 Oct 40

Effect of furosemide at various concentrations (0.05-4 mM) was examined on the in vitro biosynthesis of prostaglandins in human platelets. At lower furosemide concentrations (0.05 and 0.1 mM) no effect was observed. At 1 and 2 mM concentrations, PGE2 significantly (P less than 0.01) increased. At 3 and 4 mM concentrations PGE2 increased though not significantly probably because of the small number of samples (n=5). A decrease in PGD2 formation was noted at 1-4 mM furosemide concentrations, though significantly only at 3 mM conc. At 1 and 2 mM concentrations, TxB2 and HHT increased whereas at 3 and 4 mM concentrations these metabolites were decreased. These effects were, however, not significant. No effect was observed on endoperoxide generation at 1 and 2 mM conc. Furosemide at 1 and 2 mM concentrations inhibited ADP- and arachidonic acid induced platelet aggregation. An increased platelet formation of PGE2 in the presence of furosemide may point to the fact that this drug shows its effect mainly on the formation of PGE2 which has been found to exert a profound effect on renal blood flow and thus ameliorates some forms of hypertension.
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PMID:Effect of furosemide on the in vitro prostaglandin biosynthesis in human platelets. 681 95

Female Long-Evans hooded rats received Schroeder's rye-based diet and 0 or 1 microgram/ml cadmium, or cadmium plus lead in mineral fortified drinking water from weaning to 18 months. The heavy metal-fed rats were normal with respect to control, including growth rates and final body weights. Rats receiving added cadmium and cadmium plus lead in the diet were characterized by a persistent hypertension which was evident after 2 months. Cardiac conduction system excitability was depressed preferentially in cadmium-(atrioventricular nodal region) and cadmium plus lead-(His-Purkinje system) fed rats. Although heart rates were comparable to control, myocardial contractile activity (peak active tension and dT/dt) was significantly decreased in intact perfused heart preparations from both heavy metal-treated groups. In conjunction with the observed physiologic changes, various tissue-specific metabolic alterations were detected in heart, kidney, and liver. Generally, prolonged heavy-metal ingestion at these levels resulted in impaired energy metabolism (e.g., decreased ATP, PCr; increased Pj, ADP concentrations) and altered essential mineral composition (e.g., calcium, magnesium, zinc, and to a lesser extent, sodium and potassium; copper levels were unaffected) that varied in severity according to the tissue. The addition of lead to the cadmium diet had little additive effect on the cardiovascular system; however, renal and hepatic tissues did exhibit apparent additive effects further suggesting that cadmium and lead actions and interactions may be tissue dependent. These experimental findings and the biologic inferences derived are consonant with the hypothesis that chronic, life-long cadmium exposure approximating environmental levels may have significant adverse effects on mammalian systems, that include effects on cardiovascular tissues.
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PMID:Cardiac physiologic and tissue metabolic changes following chronic low-level cadmium and cadmium plus lead ingestion in the rat. 685 84

Defective vasodilator function could be important in the pathogenesis and/or maintenance of the hypertensive state and the predisposition of the elderly to hypertension. Impaired beta-adrenergic-mediated vasodilation and reduced lymphocyte beta-adrenergic activation of adenyl cyclase have been demonstrated both in aging and with hypertension. The cellular mechanisms responsible for these alterations remain unclear. To determine if these defects may be due to alterations in guanine nucleotide regulatory proteins (G proteins) that link receptor activation with effector function, we assessed (1) human lymphocyte adenyl cyclase activity, (2) stimulatory G proteins by cholera toxin-mediated [32P]ADP ribosylation and, in hypertensive subjects, with alpha s-specific and beta-subunit antisera, and (3) inhibitory G proteins by pertussis toxin-mediated [32P]ADP ribosylation and, in older subjects, with alpha i,1,2- and beta-subunit-specific antisera. Lymphocytes from older subjects and from hypertensive subjects demonstrated a comparable reduction in isoproterenol-stimulated adenyl cyclase. However, aluminum fluoride-stimulated activity was reduced only in lymphocytes from hypertensive subjects. Furthermore, aluminum fluoride-stimulated activity was inversely correlated with mean arterial pressure. In lymphocytes from younger hypertensive subjects, cholera toxin-mediated labeling was significantly increased. In contrast, inhibitory G protein labeling by immunodetection was unaltered. In lymphocytes from older subjects, cholera toxin-mediated labeling was not altered; however, pertussis toxin-mediated labelling was significantly increased. In contrast, inhibitory G protein labeling by immunodetection was unaltered. Overall, the study suggests alterations of G protein function of adenyl cyclase is impaired. However, these defects are associated with divergent alterations in stimulatory and inhibitory G proteins.
Hypertension 1995 Nov
PMID:G protein alterations in hypertension and aging. 759 Oct 10

In this study we examined whether the reduced fibrinolysis and increased platelet activity that are known to occur in hypertension are already present in borderline hypertension. Twelve patients with 'borderline' hypertension (diastolic blood pressure 90-95 mmHg) were found to have substantially reduced fibrinolytic activity, both at rest and during exercise, compared with 12 normotensive controls. Euglobulin clot lysis time (ECLT) was significantly higher in hypertensive subjects (218 min vs. 145 min; P < 0.05), and this difference persisted during exercise. Resting tissue plasminogen activator activity (t-PA) did not differ in the two groups, but the brisk increase in t-PA in controls during exercise (0.64 rising to 1.44 IU mL-1; P < 0.01) did not occur to the same extent in the borderline hypertensive subjects. Levels of the fast-acting t-PA inhibitor, normally referred to as PAI-1, were considerably higher in hypertensives (9.22 vs. 4.41 IU mL-1; P < 0.02), and this difference persisted in the upright posture, indicating a decrease in fibrinolytic activity. Platelet aggregability induced by ADP in vitro was not significantly higher in the hypertensive subjects, but indices of platelet activity in vivo (B-TG and PF-4 levels) revealed enhanced platelet function in the hypertensives. These results indicate that the indicators of altered haemostatic function known to occur in hypertension, namely diminished fibrinolytic activity and increased platelet function, are already detectable during the very earliest stage of the disease.
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PMID:Platelet function and fibrinolytic activity during rest and exercise in borderline hypertensive patients. 760 Dec 2

We designed this study to evaluate the effect of low versus high calcium intake on platelet function in salt-loaded patients with mild hypertension. After a 7-day period of dietary salt restriction, 19 patients were placed on a high salt (300 mmol/d), low calcium (6.25 mmol/d) diet for 7 days; 10 of these patients were given 54 mmol/d of supplementary calcium, and 9 patients were given placebo. At the end of the low and high salt regimens, we evaluated changes in blood pressure, platelet aggregation, and the platelet release reaction measured as plasma beta-thromboglobulin and platelet factor 4 levels. With high salt intake, significant increases in mean blood pressure (P < .02), red blood cell sodium (P < .01), and platelet aggregation induced by 3 mumol/L ADP (P < .01) and by 3.0 mg/L epinephrine (P < .05) were observed in the placebo-treated patients but not in the calcium-supplemented ones. Compared with the placebo-treated patients, calcium-supplemented patients had a smaller weight gain (P < .05) but excreted more sodium and calcium (P < .01) at the end of the high salt regimen. Calcium supplementation resulted in decreases in beta-thromboglobulin (P < .05), platelet factor 4 (P < .01), and plasma and urinary excretions of norepinephrine (P < .02) during the high salt, low calcium regimen. The decrease in plasma norepinephrine correlated positively with the decreases in beta-thromboglobulin (r = .72, P < .02) and platelet factor 4 (r = .85, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Jul
PMID:Calcium supplementation attenuates an enhanced platelet function in salt-loaded mildly hypertensive patients. 760 19


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