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

Left ventricular hypertrophy is the consequence of a structural adaptation of the heart in response to the chronic pressure load, leading to a reduction of the increased systolic wall stress. Studies in spontaneously hypertensive rats have shown, that left ventricular hypertrophy can be influenced by various, but not all antihypertensive agents. Alpha-methyldopa, captopril, beta-blockers and calcium channel blockers resulted in reversal of hypertrophy. Treatment with diuretics, hydralazine or minoxidil did not increase or alter degree of myocardial hypertrophy despite normalization of blood pressure. The biochemical profile after reversal of hypertrophy differs according to antihypertensive therapy, i.e. alpha-methyldopa induces an increase in collagen content, whereas captopril does not alter the collagen content of the myocardium. Adrenergic factors play an important role in modulating the response of the heart. In clinical studies the reduction in cardiac mass does not depend solely on the antihypertensive effect on blood pressure levels. There is only a weak correlation between decrease of left ventricular hypertrophy and fall of blood pressure level, as is shown in 12 patients with essential hypertension, treated with captopril over 6 months. The degree of regression of hypertrophy is influenced by stability of blood pressure control (diurnal variations and response to stress are more important than single casual values), neurohumoral response, presence of associated cardiac diseases, cause and severity of hypertension, genetic factors and age. We studied the regression of left ventricular hypertrophy by M-mode-echocardiography in 12 patients with mild or moderate essential hypertension during a 6-month therapy with captopril (50-75 mg p.d.) and hydrochlorothiazide (50 mg p.d.). In 11 of 12 patients captopril treatment resulted in a reduction of LV-mass of 30.9 +/- 15.1% and wall thickness. Peak systolic and endsystolic wall stress decreased significantly (-29.1% and -27.2%, resp.) after blood pressure reduction, but were still slightly elevated. Ejection fraction increased by 5.4% (p less than or equal to 0.05). 6 hypertensive patients treated for 6 months with metoprolol (150 mg p.d.) and hydrochlorothiazide (50 mg p.d.) do not show significant reduction of LV-mass (-6.5%). Peak and endsystolic wall stress were significantly reduced (-33.1% and -11.5%, resp.) as in captopril therapy. In 34 patients with severe hypertension treated with captopril, hydrochlorothiazide and metoprolol over 30 months, we observed a decline in the Sokolow-Lyon-Index from 4.8 +/- 1.1 mV to 3.8 +/- 0.5 mV after 6 months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Regression of left heart hypertrophy in arterial hypertension: principles, experimental and clinical findings]. 293 16

We describe diastolic properties of the myocardium in terms of stress-strain relations. In a mathematical analysis, the equation sigma = alpha(e beta.epsilon-1) of the stress-strain curve can be changed by an increase in the exponent beta or the multiplicative constant alpha. It can be experimentally shown that in hypertrophied myocardium of rats with essential hypertension and renal hypertension (SHR and Goldblatt rats, respectively), the steepening of the stress-strain curve is associated with an increase in the exponent beta (stiffness constant) and an enhancement of collagen content. On the other hand, in acute hypoxic myocardium, the slope of the stress-strain curve is increased without a significant change of the exponent beta. Our results from heat measurements and quick-release experiments indicate that the hypoxic contracture (H) and the oxygen and glucose deficiency contracture (HG) are in contrast to the results of depolarization contracture (KCl) and experimental tetanus (T). In H and HG, the cross-bridge cycling rate was found to be slowed by a factor of 2,000 compared to KCl and T. This means that ATP demand for force development and maintenance is 2,000 times less in H and HG than in KCl and T. We will further discuss the meaning and implications of these experimental findings.
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PMID:Changes in myocardial distensibility in rat papillary muscle: fibrosis, KCl contracture, hypoxic contracture, oxygen and glucose deficiency contracture, and experimental tetanus. 295 60

Arterial hypertension is considered a major risk factor in atherosclerosis in the pathogenesis of which platelet activity plays a fundamental role. However the data in the literature on platelet function in arterial hypertension do not always agree. The present study was conducted on whole blood, using the impedance metering technique to assess platelet aggregation induced by ADP (10 pg) and collagen (2 mg/ml) in 15 patients with uncomplicated essential hypertension and 25 healthy controls. Analysis of the data shows a statistically significant difference between the aggregation curves of the hypertensive and the healthy subjects with excessive platelet aggregation in those suffering from uncomplicated arterial hypertension.
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PMID:[Platelet aggregation in whole blood with the impedance method in subjects with non-complicated essential arterial hypertension]. 296 26

The spontaneously hypertensive rat (SHR)--animal model for human essential hypertension--develops a generalized arteriopathy. The present paper discusses the atherogenic influence of hypertensive arterial lesions. The following changes in the intima might influence its permeability and barrier function, increase the trapping effect and stimulate the smooth muscle cell proliferation: the hyper-reactivity of endothelial cells; the decreased thickness of endothelial cell periphery; the reduced intercellular junction pathways; the increase in basal lamina and glycosaminoglycan sub-endothelial material; the mononuclear cell infiltrations; the widened fenestrae in the internal elastic lamina. Some hypertensive changes of the tunica media may also interact with atherogenic process through reduced smooth muscle cell lipolytic capabilities, slowed transmural diffusion, perturbed efflux, aggravated media hypoxia, namely: the decrease in esterase and cholinesterase activities, the activations of some lysosomal enzymes, the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness and transmural passage; the modified smooth muscle cell behavior.
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PMID:[Hypertensive arteriopathy and atherogenesis: cellular and molecular interactions]. 310 95

The turnover of type III collagen, a major constituent of the myometrium and the uterine cervix, during pregnancy was evaluated by monitoring serum antigens related to the aminoterminal propeptide of type III procollagen. Their concentration increased markedly towards term in most uncomplicated pregnancies, while their size distribution throughout the pregnancy resembled that seen in the sera of normal healthy persons. In some patients, however, the level remained low, indicating interindividual variation in the release into serum and metabolism of the propeptide. There were no distinct changes during or immediately after vaginal delivery. Values exceeding the reference range for uncomplicated pregnancies were found during weeks 28-37 in patients with pre-eclampsia, essential hypertension, intrahepatic cholestasis of pregnancy or twin pregnancy. Thus, pregnancy should be taken into account when evaluating results of the serum assay for the aminopropeptide and the use of this assay as an indicator of pregnancy complications warrants further study.
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PMID:Collagen metabolism in normal and complicated pregnancy: changes in the aminoterminal propeptide of type III procollagen in serum. 310 54

The effects of chronic therapy, using an angiotensin converting enzyme (ACE) inhibitor (S9490-3 perindopril, 1 mg/kg), on the mechanical and structural properties of large arteries were studied in two-kidney, one clip (2K, 1C) Goldblatt hypertensive and spontaneously hypertensive rats (SHR) compared with matched normotensive Wistar and Wistar-Kyoto (WKY) animals. The treatment was carried out for 1 month in Goldblatt-hypertensive rats and 3 months in SHR, i.e. for 1 month after blood pressure was normalized. At the end of the treatment period the passive mechanical properties of the isolated carotid artery were measured in situ. Carotid compliance was calculated from the pressure-volume relationship between 50 and 250 mmHg. Morphological parameters of the aortic wall, including medial thickness, nucleus density and elastin and collagen content, were recorded by an automated morphometric system. Renal and essential hypertension were associated with a shift of the passive pressure-volume relationship in the carotid, corresponding to a decrease in arterial compliance. The passive mechanical properties of the carotid were normalized by ACE inhibitor treatment in renovascular hypertensive rats but remained unchanged in chronically treated SHR. The ACE inhibitor completely reversed the medial hypertrophy in Goldblatt-hypertensive rats but the reversal of medial hypertrophy was incomplete in SHR. The elastin to collagen ratio in the aortic media was significantly increased by 3 months of treatment with the ACE inhibitor in the SHR and WKY groups but remained unchanged in the Goldblatt-hypertensive and Wistar rats treated for 1 month.
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PMID:Arterial effects of angiotensin converting enzyme inhibition in renovascular and spontaneously hypertensive rats. 322 86

The platelet-activating effect of low-density lipoprotein, ADP and collagen was investigated in 45 essential hypertensive patients (27 men, 18 women) and 45 healthy normotensive subjects strictly matched for age and sex. No differences in mean values were found between essential hypertensive and normotensive subjects. However, in essential hypertensive patients platelet sensitivity to low-density lipoprotein correlated positively whereas ADP and collagen correlated negatively with blood pressure (P less than 0.05). Diminished platelet sensitivity to ADP and collagen may reflect receptor desensitization. The pressure-dependent increase in platelet response to low-density lipoprotein possibly contributes to enhanced thrombo-embolic complications and platelet-mediated vasoconstriction as well as to low-density lipoprotein-related vascular damage in essential hypertension.
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PMID:Low-density lipoprotein enhances platelet activation in parallel with the height of blood pressure. 324 Dec 77

The present study examines the putative role of serotonin (5-hydroxytryptamine) in the pathogenesis of essential hypertension. Intraplatelet and plasma free serotonin levels, as well as the amounts released from aggregating platelets, were measured in six patients with untreated essential hypertension, using high performance liquid chromatography with electrochemical detection. Platelet serotonin contents were similar to those in age-matched controls. However, hypertensive patients showed significantly higher levels of plasma free serotonin as well as a significantly higher release from aggregating platelets, stimulated by collagen or adenosine diphosphate (ADP). These data suggest that serotonin may be involved in the pathogenesis of essential hypertension.
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PMID:Serotonin levels in hypertension. 345 3

Vascular changes in the mesenteric arteries were examined in three animals models for human essential hypertension. These models are: spontaneously hypertensive rats, which develop hypertension with age; Dahl model of genetic, salt-dependent hypertensive rats; and deoxycorticosterone-salt hypertensive rats. Morphometric measurements of the arterial wall components (e.g., endothelium, media) were carried out in the elastic arteries, muscular arteries, and arteriolar vessels from the mesenteric bed. The observed changes were correlated with the stages of hypertension development and the effect of antihypertension therapy, including sympathectomy. Specific emphasis was made to determine whether the changes observed were primary in nature, and related to the causes of hypertension, or they were secondary adaptive changes. A comparison of the three models showed that common changes in the intima, media, and adventitia were present in the three models. Alterations in the endothelium (e.g., enlargement of subendothelial space, necrotic changes), adventitia (collagen increase), and hypertrophy of the smooth muscle cells are secondary adaptive changes, because these changes occur subsequent to the development of hypertension, and antihypertensive therapy also prevent these changes from taking place. In contrast, hyperplasia of the smooth muscle cells is a primary change, because it occurs prior to the onset of hypertension. Functionally, alteration in the media is probably the most important change, because it can cause hyperreactivity of the arteries in response to stimulation. Damage to the endothelial cells may play a role in the maintenance of hypertension during the later phase. Alteration in adventitia is a passive change, which does not appear to have a major role in hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Structural alterations of blood vessels in hypertensive rats. 369 Mar 88

The effects of a calcium antagonist nifedipine (Adalat) on platelet aggregation was examined in vitro and in vivo. In vitro examination: Platelet aggregation induced by adenosine disphosphate (ADP), epinephrine, collagen, arachidonate, and thrombin was all inhibited dose-dependently in the platelet-rich plasma prepared from the blood of healthy individuals by the addition of nifedipine to a final concentration of 5 or 10 micrograms/ml. In vivo examination: 20 patients with essential hypertension were treated with 30 mg/d of nifedipine for 8 weeks. Significant decreases in both systolic and diastolic pressures were observed 2 weeks after the beginning of the administration, and continued throughout the administration period. ADP-induced platelet aggregation decreased by 25% after 2 weeks, 36% after 4 weeks, and 44% after 8 weeks (p less than 0.05 for all decreases). Plasma thromboxane B2 level also decreased markedly from 217.3 +/- 91.7 pg/ml before the administration to 119.0 +/- 29.7 pg/ml (p less than 0.01) 2 weeks after, and 99.1 +/- 25.4 pg/ml (p less than 0.01) 8 weeks after the beginning of the administration, suggesting suppressed thromboxane A2 production.
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PMID:Effects of the calcium antagonist nifedipine on thromboxane B2 level and platelet aggregation in hypertensive patients. 381 28


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