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)

Islet-activating protein (IAP), pertussis toxin, is an oligomeric protein composed of an A-protomer and a B-oligomer. There seem to be at least two molecular mechanisms by which IAP exerts its various effects in vivo and in vitro. On the one hand, some of the effects were not significantly affected by acetamidination of the epsilon-amino groups of the lysine residues in the molecule. These include the activities in vitro (1) catalyzing ADP-ribosylation of one of the membrane proteins directly, (2) enhancing membrane adenylate cyclase activity in C6 cells, (3) reversing receptor-mediated inhibition of insulin or glycerol release from pancreatic islets or adipocytes, respectively, and the activities in vivo (4) inhibiting epinephrine-induced hyperglycemia, (5) potentiating glucose-induced hyperinsulinemia, (6) reducing hypertension and increasing the heart rate in genetically hypertensive rats. These activities are concluded to develop as a result of ADP-ribosylation catalyzed by the A-protomer which is rendered accessible to its intramembrane substrate thanks to the associated B-oligomer moiety. Thus, neither the enzymic activity of the A-protomer nor the transporting activity of the B-oligomer needs free amino groups of the lysine residues in the IAP molecule. On the other hand, additional effects of IAP, such as (1) mitogenic, (2) lymphocytosis-promoting, (3) histamine-sensitizing, (4) adjuvant and (5) vascular permeability increasing, were markedly suppressed by acetamidination of the intrapeptide lysine residues. The free epsilon-amino group of lysine would play an indispensable role in the firm (or divalent) attachment of the B-oligomer of IAP to the cell surface that is responsible for development of these activities.
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PMID:Dual mechanisms involved in development of diverse biological activities of islet-activating protein, pertussis toxin, as revealed by chemical modification of lysine residues in the toxin molecule. 638 83

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

The influence of 7-[2-hydroxy-3-(N-2-hydroxyethyl-N-methylamino)propyl]-1, 3-dimethyl-xanthine-pyridine-3-carboxylate (xantinol nicotinate, Complamin) on brain metabolism was studied in the following test models: 1. determination of glucose-14C permeation in rats with experimental nephrogenic hypertension; 2. determination of the intercerebral ATP-concentration in ischaemic rats; 3. determination of the adenosine triphosphate (ATP) pool in healthy rats; 4. evaluation of the incorporation rates of 32Pi-isotope into the adenosine phosphates of the rat brain. The results of these studies show, that the reduced glucose permeation rates in rats with nephrogenic hypertension can be normalized by xantinol nicotinate above values of controls. In hypoxemic rats it could be shown, that xantinol nicotinate antagonizes the decrease of the intracerebral ATP-concentration by 50%. The investigation of the ATP-pool resulted in a significant increase of the ATP level in the brain tissue about 35% at maximum. This increase of the ATP-concentration continues up to 4 h following a single oral administration of xantinol nicotinate. The determination of the incorporation rates of 32Pi-isotope showed that only small amounts of radioactivity were measured in the AMP-fraction in controls as well as in xantinol nicotinate treated rats. Further phosphorylation steps of adenosine monophosphate (AMP) to adenosine diphosphate (ADP) and ATP, however, are considerably activated by xantinol nicotinate, whereby maximum labelling rates of the ADP were found already 15 min after dosing. Maximum 32Pi-incorporation rates of the ATP-fraction were measured 30 min following administration of the tracer and of xantinol nicotinate, respectively.
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PMID:[Effect of xanthinol nicotinate on brain metabolism in rats]. 668 47

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

Since 1966, 29 patients with recurrent carotid artery stenosis have been encountered. The mean (+/- SEM) internal between initial carotid endarterectomy and secondary presentation was 67.5 +/- 9.2 months (range 6 to 180 months). There was a disproportionate number of women with recurrent stenosis. The mean age at initial endarterectomy in patients with recurrent stenosis, 54.6 +/- 1.4 years, was significantly less (P less than 0.001) than that of all patients who had endarterectomy. To define the etiologic factors for recurrence, 21 of these patients were matched with case-control patients of the same age and sex who had undergone endarterectomy the same year but did not develop recognized recurrent stenosis. There was no significant difference in the incidence of hypertension, diabetes mellitus, coronary artery disease, bilateral carotid disease, other vascular operations, or family history for atherosclerosis in patients with recurrent stenosis compared to control patients. The indications for primary endarterectomy, angiographic distribution of disease, and operative details were similar in both groups. There was no difference in the incidence of regular, therapeutic aspirin ingestion following initial endarterectomy (52.5% in both groups). There was a striking difference in smoking habits. Ninety-five percent of patients with recurrent stenosis continued to smoke following initial endarterectomy, compared to 23.8% of control patients (P less than 0.001). Lipid fractionation studies were performed in both groups, and there were no significant differences in levels of cholesterol, triglycerides, high-density lipoprotein (HDL)-cholesterol, and total cholesterol/HDL-cholesterol ratio. Dose-response platelet aggregometry detected no differences between groups in the sensitivity of platelets to adenosine diphosphate (ADP), collagen, and epinephrine. Reoperation in patients with recurrent stenosis was associated with minimal morbidity, no deaths, and generally excellent results.
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PMID:Etiologic factors for recurrent carotid artery stenosis. 682 70

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


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