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1. |
Looking back on three years of Editorship |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 1-1
Alberto Zanchetti,
Giuseppe Mancia,
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ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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2. |
Sodium‐lithium countertransportphysiology and function |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 3-13
Ian West,
Peter Rutherford,
Trevor Thomas,
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摘要:
Current opinions on the relationships between erythrocyte sodium-lithium countertransport kinetics and primary hypertension, hyperlipidaemia and diabetic nephropathy are reviewed. Problems associated with the assay are analysed. Some possible mechanisms that could modify the kinetics of ion exchange are examined. The question of what catalyses sodium-lithium countertransport is discussed, but not answered. Some models are put forward showing how a study of sodium-lithium countertransport kinetics could further our understanding of important disease processes.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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3. |
Should exercise blood pressure be measured in clinical practice? |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 15-17
Tien Tsao,
David Wright,
Lip Tan,
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ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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4. |
Clustering of coronary risk factors with increasing blood pressure at rest and during exercise |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 19-22
Reidar Mundal,
Sverre Kjeldsen,
Leiv Sandvik,
Gunnar Erikssen,
Erik Thaulow,
Jan Erikssen,
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摘要:
BackgroundThe metabolic cardiovascular syndrome is the label given to the clustering of unfavourable levels of a number of coronary risk factors in subjects with high resting blood pressures. We found recently that exercise blood pressure had a strong independent prognostic value.ObjectiveTo search for possible similar associations between exercise blood pressure levels and coronary risk factors by studying conventional and recently acknowledged coronary risk factors.MethodsThe study population comprised 1999 healthy men aged 40–59 years. Age-adjusted coronary risk factor levels and their relation to resting and exercise blood pressures were studied. Resting blood pressure was measured after subjects had rested supine for 5 min. The exercise blood pressure used was the systolic blood pressure measured with the subject sitting on a bicycle ergometer at the end of a work load of 600 kpm/min (100 W) for 6 min.ResultsBesides corroborating the relation between the metabolic syndrome and resting blood pressure levels, we observed similar or even stronger associations between levels of various coronary risk factors and exercise blood pressure. We found rather strong, direct associations between exercise blood pressure and total cholesterol level, fasting triglyceride level and body mass index whereas inverse relations were found for glucose tolerance, physical fitness, pulmonary functioning and the ability to increase heart rate during exercise. Virtually all these associations had a level of statistical significance of P < 0.001.ConclusionsHigh exercise blood pressure levels are strongly associated with unfavourable levels of a number of important coronary risk factors. A similar metabolic syndrome to that observed in subjects with high resting blood pressures therefore appears to be present in subjects with high exercise blood pressure responses. These associations may considerably amplify the independent risk of high blood pressure responses to moderate exercise.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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5. |
Limitations of the difference between clinic and daytime blood pressure as a surrogate measure of the ‘white‐coat’ effect |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 23-29
Gianfranco Parati,
Stefano Omboni,
Jan Staessen,
Lutgarde Thijs,
Robert Fagard,
Luisa Ulian,
Giuseppe Mancia,
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摘要:
BackgroundThe difference between clinic and ambulatory average daytime blood pressures is frequently taken as a surrogate measure of the ‘white-coat effect’ (i.e. the pressor reaction triggered in the patient by the physician's visit).ObjectiveTo assess the reproducibility of this difference and its relationship with clinic and average ambulatory daytime blood pressure levels.Design and methodsThese issues were addressed with two large groups of subjects in whom both clinic and ambulatory blood pressures were measured, namely 783 outpatients with systolic and diastolic essential hypertension [Group 1, aged 50.8 ± 9.4 years (mean ± SD)], participating in standardized Italian trials of antihypertensive drugs, and 506 elderly patients (group 2, age 71 ± 7 years) with isolated systolic hypertension, participating in the European Syst-Eur trial.ResultsThe clinic-daytime blood pressure difference for the essential systolic and diastolic hypertensive patients (group 1) was 13.6 ± 14.3 mmHg for systolic and 9.1 ± 8.6 mmHg for diastolic blood pressure (Palways < 0.01). This difference for the elderly patients with isolated systolic hypertension (group 2) was 21.2 ± 16.0 mmHg for systolic and only 1.3 ± 10.2 mmHg for diastolic blood pressure (P< 0.01 andP< 0.05, respectively). In both studies little or no systematic clinic-daytime difference could be observed for heart rate. The reproducibility of the clinic-daytime blood pressure difference, tested for 108 essential systolic and diastolic hypertensive patients from group 1 and 128 isolated systolic hypertensives from group 2, was invariably lower than that both of daytime and of clinic blood pressure values. Finally, the clinic-daytime blood pressure difference was progressively higher for increasing levels of clinic blood pressure and progressively lower for higher levels of ambulatory daytime blood pressure.ConclusionsThus, the clinic-daytime blood pressure difference has a limited reproducibility; depends not only on clinic but also on daytime average blood pressure, which means that its size is a function of the blood pressure criteria employed for selection of the patients in a trial; and is never associated with a systematic clinic-daytime difference in heart rate, which further questions its use as a reliable surrogate measure of the true pressor response induced in the patient by the doctor's visit.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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6. |
Nitric oxide synthase gene polymorphisms, blood pressure and aortic stiffness in normotensive and hypertensive subjects |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 31-35
Patrick Lacolley,
Sylvie Gautier,
Odette Poirier,
Bruno Pannier,
François Cambien,
Athanase Benetos,
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摘要:
BackgroundGenetic studies may help us to understand the mechanisms underlying the involvement of various neuro-humoral factors in the regulation of the mechanical properties of large arteries. We have shown previously that the angiotensin II type 1 receptor gene polymorphism was a strong determinant of aortic stiffness in hypertensives.ObjectiveTo assess the contribution of two polymorphisms of the endothelial nitric oxide synthase gene to aortic stiffness in normotensive and hypertensive subjects in the same cohort.MethodsWe studied 309 untreated hypertensive and 123 normotensive subjects. Aortic stiffness was evaluated by measuring the carotid-femoral pulse-wave velocity non-invasively. The endothelial nitric oxide synthase gene polymorphisms G10-T at intron 23 (GIN23T) and G298-T at exon 7 (Glu298Asp) were determined in each subject.ResultsThe distributions of genotypes and allele prevalences of the endothelial nitric-oxide synthase G10-T polymorphisms among hypertensive and normotensive subjects were similar. In contrast, the prevalence of the nitric oxide synthase298G allele was higher in the hypertensive group than it was among normotensive subjects. We found no association of the endothelial nitric oxide synthase genotypes with blood pressure levels or pulse-wave velocity for either population.ConclusionsThe present results do not suggest that two common polymorphisms of the endothelial nitric oxide synthase gene are involved in the regulation of aortic stiffness in hypertensive and normotensive individuals. The higher prevalence of endothelial nitric oxide synthase298G allele among hypertensives suggests that this gene is involved in essential hypertension but this observation needs further confirmation.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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7. |
Gene polymorphisms of the renin‐angiotensin system in relation to hypertension and parental history of myocardial infarction and strokethe PEGASE study |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 37-44
Laurence Tiret,
Hervé Blanc,
Jean-Bernard Ruidavets,
Dominique Arveiler,
Gérald Luc,
Xavier Jeunemaitre,
Jean Tichet,
Christine Mallet,
Odette Poirier,
Pierre-François Plouin,
François Cambien,
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摘要:
ObjectiveTo investigate a possible involvement of polymorphisms of the renin-angiotensin system in predisposition to moderate and severe hypertension and their relationship to parental histories of myocardial infarction and stroke.MethodsHypertensive cases (453 men, 326 women) were patients followed up by general practitioners for established hypertension. Inclusion criteria were an age of onset of hypertension < 60 years and a diastolic blood pressure > 105 mmHg without antihypertensive medication or > 100 mmHg under treatment. Normotensive controls were selected from population-based samples (362 men) and during a preventative medicine visit (170 women). Polymorphisms of the angiotensinogen gene (AGT M235T and T174M), the angiotensin I converting enzyme gene (ACE I/D), and the angiotensin II type 1 receptor gene (AGT1R A1166C) were investigated.ResultsThe AGTT235allele prevalence was higher among male hypertensive cases than it was among controls (0.46 versus 0.40,P= 0.01) and a similar trend was observed with female cases whose hypertension had been diagnosed before they were aged 45 years (0.44 versus 0.38,P= 0.20). The AGT1RC1166allele prevalence was higher among female hypertensives than it was among controls (0.30 versus 0.23,P= 0.03) but no such difference was observed for men. The AGT T174M and ACE I/D polymorphisms were not associated with hypertension. Hypertensive patients reporting a parental history of myocardial infarction before age 60 years had a higher prevalence of the ACEDallele than did those without such a parental history (0.68 versus 0.56,P= 0.01). The ACEDallele prevalence was also greater among patients reporting a parental history of stroke incidence before age 65 years (0.66 versus 0.57,P= 0.05).ConclusionsThese results support the hypothesis that the AGT gene plays a role in predisposition to hypertension and that the ACE gene plays a role in predisposition to acute ischemic events.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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8. |
Progressive vascular damage in hypertension is associated with increased levels of circulating P‐selectin |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 45-50
Marianne Verhaar,
Jaap Beutler,
Carlo Gaillard,
Hein Koomans,
Rob Fijnheer,
Ton Rabelink,
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摘要:
ObjectiveTo assess whether increased shedding of adhesion molecules in plasma provides an index for endothelial damage in hypertension.Design and methodsThree groups of hypertensive patients with increasing severity of vascular damage were studied: 20 essential hypertensives, 21 atherosclerotic, renovascular hypertensives and four malignant hypertensives. Twenty healthy subjects were included as a control group. Levels of P-selectin, E-selectin, intracellular adhesion molecule 1, vascular cell adhesion molecule and von Willebrand factor in venous blood were measured, using sandwich-type enzyme-linked immunosorbent assay.ResultsFor essential hypertensives a trend for increased P-selectin and E-selectin values compared with those in controls was observed (159 ± 44 versus 132 ± 40 ng/ml,P= 0.062 and 40 ± 13 versus 34 ± 17 ng/ml,P= 0.055, respectively). P-selectin (210 ± 84 ng/ml,P= 0.0021) and E-selectin (42 ± 12 ng/ml,P= 0.012) levels in renovascular hypertensives were significantly higher than those in healthy controls. There were no significant increases in circulating levels of intracellular adhesion molecule 1, vascular cell adhesion molecule and von Willebrand factor either in essential hypertensives or in renovascular hypertensives. Marked increases in circulating levels of adhesion molecules and von Willebrand factor relative to those in controls were observed in malignant hypertensives (P-selectin 634 ± 332 versus 132 ± 40 ng/ml,P= 0.0004; vascular cell adhesion molecule 968 ± 187 versus 493 ± 139 ng/ml,P= 0.0004; and von Willebrand factor 259 ± 75 versus 130 ± 72 U/dl, P = 0.016).ConclusionsProgression of vascular damage in essential, renovascular and malignant hypertension is associated with a rise in circulating levels of P-selectins and, to a lesser extent, E-selectins, whereas levels of intracellular adhesion molecule 1, vascular cell adhesion molecule and von Willebrand factor are elevated only in diseases associated with acute severe vascular damage, including malignant hypertension. Our data suggest that selectins may be useful as indicators of vascular damage in hypertension.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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9. |
Single pericytes and pericytes in suspension are stimulated in a similar way by low‐density lipoprotein |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 51-54
Sven Skinner,
Eva Niederer,
Rudolf Locher,
Wilhelm Vetter,
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摘要:
BackgroundPericytes are regarded as the microvascular counterpart of smooth muscle cells and implicated in the regulation of blood pressure at the microvascular level. Ca2+plays an important role in biochemical processes involved in blood pressure regulation and can be activated by low-density lipoprotein (LDL) cholesterol.ObjectiveTo determine whether stimulation either of single cells or of cells in suspension by LDL would produce any difference in the increase in cytosolic free calcium levels ([Ca2+]i).Design and methodsSingle pericytes were loaded with 2 μmol/l of the Ca2+-sensitive dye Indo-1/AM. The Indo-1 fluorescence was recorded at 405 nm (Ca2+-bound) and 485 nm (Ca2+-free) after stimulation with LDL. Pericytes in suspension were loaded with 2 μmol/l of the Ca2+-sensitive dye FURA-2/AM. The FURA-2 fluorescence kinetics were recorded at 340–380 nm. Ratios of fluorescence at the two wavelengths were transformed to [Ca2+]i.ResultsBasal [Ca2+]ilevels appeared to be higher in single cells (148 ± 13 nmol/l, n = 20) than they were in cells in suspension (128 ± 8 nmol/l, n = 25;P= 0.0078). After stimulation with LDL the increase in [Ca2+]iin both systems was about 220% above baseline. A clear dose dependency was seen for both systems.ConclusionsSingle pericytes and pericytes in suspension increase their [Ca2+]iafter stimulation with LDL dose-dependently. Even though single-cell measurements revealed some technical limitations, their responses were comparable to those obtained in a cell suspension. In analogy to aortic smooth muscle cells, our results indicate that LDL might also play a blood-pressure-regulatory role in the microvasculature.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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10. |
Lack of autonomic contributions to tonic nitric oxide‐mediated vasodilatation in unanesthetized free‐moving rats |
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Journal of Hypertension,
Volume 16,
Issue 1,
1998,
Page 55-61
Alberto Radaelli,
Luca Mircoli,
Stefano Perlini,
Gianni Bolla,
Ileana Mori,
Giuseppe Mancia,
Alberto Ferrari,
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摘要:
ObjectiveTo clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers.MethodsChronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors.ResultsBaseline mean arterial pressure was 100 ± 4 mmHg (mean ± SEM) in control rats and 73 ± 3, 62 ± 5, and 105 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38 ± 3 mmHg in control rats and 51 ± 3, 50 ± 6, and 63 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats.ConclusionsTonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.
ISSN:0263-6352
出版商:OVID
年代:1998
数据来源: OVID
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