摘要:

Arterial hypertension can provoke a reduction in coronary flow reserve through several mechanisms that are not mutually exclusive (i.e. epicardial coronary artery disease (CAD), left ventricular hypertrophy and structural and/or functional microvascular disease). These different targets of arterial hypertension should be explored with different diagnostic markers. In fact, stress-induced wall motion abnormalities are highly specific for angiographically assessed epicardial CAD, whereas ST segment depression and/or myocardial perfusion abnormalities are frequently found with angiographically normal coronary arteries associated with left ventricular hypertrophy and/or microvascular disease. Exercise-electrocardiography stress test can be used to screen patients with negative maximal test due to its excellent negative predictive value, which is high and comparable in normotensives and hypertensives. When exercise-electrocardiography stress test is positive (or uninterpretable or ambiguous), an imaging stress-echo test is warranted for a reliable identification of significant, prognostically malignant epicardial CAD in view of an ischemia-guided revascularization.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTracking of blood pressure (BP) from childhood occurs in populations but, for individuals, prediction of adult BP from childhood levels is poor. We examined factors that may influence tracking of BP to identify better predictors of higher BP in early adult life.DesignA prospective study of children recruited at the age of 9 years by random sampling of Perth metropolitan schools stratified by socio-economic status.SettingCommunity based with re-surveys 3-yearly for 9 years.ParticipantsA total of 516 boys and 520 girls at 9 years; 680 boys and 630 girls at 12 years; 318 boys and 300 girls at 15 years; 330 men and 326 women at 18 years.Main outcome measuresSystolic (SBP) and diastolic (DBP) BP.ResultsPersistence in the highest quartile for SBP between surveys was seen in 34–48% of subjects and in 37% between the ages of 9 and 18 years. The proportion increased to around 60% in those in the highest quartile for body mass index (BMI), to 70% in those in the highest quartile for change in BMI and to 60% if there was a family history of hypertension. In log-linear models, persistence in a quartile for SBP was significantly related to a family history of hypertension, previous SBP, BMI and change in BMI. Relationships were similar for DBP.ConclusionsExcessive weight gain in adolescence and a family history of hypertension substantially increase the risk of higher BP persisting into early adult life. Recognition of children at risk would allow early intervention emphasizing weight control with potential long-term benefits.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo evaluate the usefulness of blood pressure and its variability in the prediction of future blood pressure and need for antihypertensive medication.MethodsWe used WHO criteria to classify, at baseline, 97 healthy untreated male volunteers as normotensive (n= 34), borderline hypertensive (n= 29) or mild hypertensive (n= 34), with casual measurements before intra-arterial 24 h ambulatory blood pressure monitoring. After 10 years of follow-up, 87 of the men (90%) were available and their blood pressure was recorded using casual measurements and non-invasive ambulatory 24 h monitoring.ResultsDuring the follow-up, the blood pressure classification deteriorated in 35 individuals (40%) and improved in six (7%) (McNemar test,P<0.0001). In the borderline hypertensive group, 77% became hypertensive (P= 0.03). The 24 h mean systolic blood pressure was the best predictor of follow-up casual systolic (adj.R2= 0.420) and 24 h systolic (adj.R2= 0.540) blood pressure. The 24 h mean diastolic blood pressure was the best predictor of follow-up casual diastolic (adj.R2= 0.301) and 24 h diastolic (adj.R2= 0.292) blood pressure. The baseline casual systolic blood pressure also predicted the follow-up casual systolic blood pressure relatively well (adj.R2= 0.356), but was clearly weaker for the follow-up 24 h systolic (adj.R2= 0.275) blood pressure. The prediction of follow-up casual diastolic (adj.R2= 0.259) and follow-up 24 h diastolic (adj.R2= 0.214) blood pressure by baseline casual blood pressure was even weaker. The means and variabilities of the 24 h, daytime, and night-time blood pressures were the best predictors of the need for antihypertensive medication (Cox–Snell R2= 0.399). The characteristics of the individual did not significantly predict future blood pressure and the need for antihypertensive medication.ConclusionsThe 24 h mean blood pressure was an excellent predictor of the future blood pressure and the need for antihypertensive medication. Prediction of antihypertensive medication was further improved by also using blood pressure variability. Systolic blood pressure was more predictable than diastolic blood pressure.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

BackgroundAlthough age is associated with increasing blood pressure, there is a substantial heterogeneity within a certain birth cohort. Whether increase in systolic and diastolic blood pressure is related to pulmonary function is largely unknown.ObjectiveTo study blood pressure elevation between 55 and 68 years of age in relation to vital capacity (VC) and forced expiratory volume (FEV1.0) at 55.DesignPopulation-based cohort study.ParticipantsA total of 375 men without antihypertensive medication at baseline.Main outcome measureChange in systolic blood pressure (SBP) and diastolic blood pressure (DBP) over 13 years.ResultsBlood pressure increase between 55 and 68 years was highest among men who at 55 years had low vital capacity. Average increase in systolic blood pressure for men with vital capacity in the first, second, third and fourth quartile was 20.4, 18.7, 16.5 and 11.1 mmHg, respectively (Pfor trend = 0.005). Average increase in diastolic blood pressure was 10.6, 9.9, 9.0 and 6.3 mmHg, respectively (P= 0.02). The trends remained statistically significant after adjustments for baseline blood pressure, tobacco consumption, smoking cessation between 55 and 68, weight change between 55 and 68, physical activity and diabetes. Further analysis showed that the relationships could be found among men with blood pressures ⩽ 140/90 mmHg at baseline, whereas no significant association was found for men whose baseline SBP or DBP exceeded 140/90 mmHg. FEV1.0 showed similar associations with change in blood pressure.ConclusionLung function is inversely associated with future blood pressure increase. It is suggested that this association could contribute to the relationships between lung function and incidence of cardiovascular disease.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo investigate the association of serum uric acid level with the risk for hypertension and Type 2 diabetes.DesignProspective cohort study.SettingWork site in Osaka, Japan.ParticipantsA total of 6356 Japanese men, aged 35–60 years with systolic blood pressure<140 mmHg and diastolic blood pressure<90 mmHg, normal glucose intolerance, and no history of hypertension or diabetes at baseline.Main outcome measuresBlood pressure was measured by standard techniques, using 160/95 mmHg for diagnosis of hypertension. Type 2 diabetes was defined as a fasting plasma glucose level⩾126 mg/dl or a 2 h post–loaded plasma glucose level⩾200 mg/dl.ResultsDuring the 61 716 person–years follow-up period, we confirmed 639 cases of hypertension and 454 cases of Type 2 diabetes. Serum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes. After adjustment for known risk factors, including daily alcohol consumption, the serum uric acid level was associated with an increased risk for hypertension; the relative risks for hypertension were 1.00 for quintile 1 of the serum uric acid level, 1.24 [95% confidence interval (CI), 0.94–1.65] for quintile 2, 1.34 (CI, 1.03–1.76) for quintile 3, 1.76 (CI, 1.35–2.29) for quintile 4, and 2.01 (CI, 1.56–2.60) for quintile 5 (Pfor trend<0.001). Even among both non-drinkers and lean subjects, serum uric acid level was associated with an increased risk for hypertension.ConclusionsSerum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo estimate the contribution of heredity to the variance in left ventricular mass (LVM), and to ascertain whether genetic factors may interact with non-genetic factors in promoting LVM growth.Subjects and settingThe study population consisted of 290 healthy parents and 251 healthy children living in Tecumseh, Michigan, USA.Main outcome measureCorrelation of parents’ LVM with offspring's LVM adjusting for a number of clinical variables.MethodsLVM in parents and offspring was measured with M-mode echocardiography by the same investigators.ResultsParents unadjusted LVM was unrelated to offspring unadjusted LVM , but after removing the confounding effect of age, sex, anthropometric measurements, systolic blood pressure, plasma insulin and urinary sodium excretion, parent–child correlation for LVM was 0.28 (P= 0.006). The relative contribution of parental-adjusted LVM and of several offspring phenotypic and environmental variables on offspring LVM was evaluated by multivariable regression analysis. When age, gender, anthropometric measurements and systolic blood pressure were accounted for, adjusted LVM of parents explained only 1.6% of the total variance in offspring LVM. However, after inclusion of insulin and urinary sodium in the model heredity explained 7.6% of the total variance in offspring LVM, and its predictive power was second only to that of child's height. Furthermore, an interactive effect of parental LVM with offspring systolic blood pressure was found on child's left ventricular mass.ConclusionHeredity can explain a small, but definite proportion of the variance in LVM. Higher blood pressure favors the phenotypic expression of the genes that regulate LVM growth.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

BackgroundSeveral indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension.ObjectiveTo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat.Design and methodsThe abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined.ResultsThe abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renalnNOSgene expression in Dahl rats with that in salt-insensitive Sprague–Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague–Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague–Dawley rats.ConclusionThese data suggest thatnNOSgene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

BackgroundPeroxynitrite (ONOO−), the product of superoxide and nitric oxide, seems to be involved in vascular alterations in hypertension.ObjectivesTo evaluate the effects of ONOO−on endothelium-dependent and independent aortic vascular responsiveness, oxidized/reduced glutathione balance (GSSG/GSH), malondialdehyde aortic content, and the formation of 3-nitrotyrosine (3-NT), a stable marker of ONOO−, inN-acetylcysteine (NAC)-treated normotensive Wistar–Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).ResultsIn SHR only, NAC significantly reduced heart rate and systolic, but not diastolic, blood pressure. It also improved endothelium-dependent aortic relaxation in SHR, but not after exposure to ONOO−. Endothelium-dependent and independent aortic relaxations were markedly impaired by ONOO−in both strains of rat. NAC partially protected SHR against the ONOO−-induced reduction in endothelium-independent relaxation. Aortic GSSG/GSH ratio and malondialdehyde, which were higher in SHR than in WKY rats, showed a greater increase in SHR after exposure to ONOO−. NAC decreased GSSG/GSH and malondialdehyde in both strains of rat before and after exposure to ONOO−. The 3-NT concentration, which was similar in both strains of rat under basal conditions, was greater in SHR than in WKY rats after the addition of ONOO−, with a reduction only in NAC-treated SHR.ConclusionsThese findings suggest an increased vulnerability of SHR aortas to the effects of ONOO−as compared with those of WKY rats. The selective improvements produced by NAC, in systolic arterial pressure, heart rate, aortic endothelial function, ONOO−-induced impairment of endothelium-independent relaxation, aortic GSSG/GSH balance, malondialdehyde content and 3-NT formation in SHR suggest that chronic administration of NAC may have a protective effect against aortic vascular dysfunction in the SHR model of hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveWe tested the hypothesis that increased responsiveness of phospholipase D (PLD) to angiotensin II (Ang II) is associated with increased oxidative stress and exaggerated growth responses in vascular smooth muscle cells (VSMC) from untreated essential hypertensive patients.DesignVSMCs from peripheral resistance arteries of normotensive and hypertensive subjects were studied. Production of reactive oxygen species (ROS) was measured with the fluoroprobe 5-(and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate (CM-H2DCFDA). PLD and reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidase were assessed with the inhibitors, dihydro-d-erythro-sphingosine (sphinganine) and diphenylene iodinium (DPI), respectively, and protein kinase C (PKC) effects were determined using chelerythrine chloride and calphostin C. PLD activity was measured by the transphosphatidylation assay.ResultsAng II increased the CM-H2DCFDA fluorescence signal, derived predominantly from H2O2. Ang II-induced generation of DPI-inhibitable ROS was significantly enhanced in cells from hypertensives compared with normotensives (Emax= 72±2 versus 56.9±1.8 fluorescence units,P<0.01). PLD inhibition attenuated Ang II-induced ROS generation, with greater effects in the hypertensive group than the normotensive group (Δ= 42±3.3 versus 21±2 units). PKC inhibition partially decreased Ang II-elicited signals. Ang II-stimulated PLD activity and DNA and protein synthesis were significantly greater in cells from hypertensives than normotensives. These effects were normalized by DPI and sphinganine.ConclusionsOur results suggest that in essential hypertension enhanced oxidative stress and augmented growth-promoting actions of Ang II are associated with increased activation of PLD-dependent pathways. These processes may contribute to vascular remodeling in hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectivesTo examine the role of endogenous nitric oxide (NO) in the pathogenesis of hypertension and insulin resistance in chronic hyperinsulinemic rats.MethodsSustained hyperinsulinemia was achieved by insulin infusion (21.5 pmol/kg per min) via subcutaneous osmotic minipump for 6 weeks. NO synthase inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME, 5 mg/kg per day) was given orally after 4 weeks of vehicle or insulin infusion. The systolic blood pressure (SBP) was measured under conscious state by an electrosphygmomanometer before and after drug treatments.ResultsInsulin infusion alone significantly increased SBP from 134±3 to 156±2 mmHg by week 4 and further to 158±3 mmHg by week 6 of insulin infusion. The insulin-infused rats had markedly decreased insulin sensitivity, as reflected by an elevated steady-state plasma glucose level estimated by the insulin suppression test. There were no significant differences in plasma glucose and triglyceride levels between rats with and without insulin infusion. When hypertension had been established in rats receiving insulin infusion for 4 weeks, superimposed l-NAME on insulin infusion for additional 2 weeks further increased SBP by 18±2 mmHg (from 157±2 to 175±2 mmHg). Plasma levels of NO metabolites (NOx) significantly decreased from 13.7±1.1 μmol/l during the control period to 6.1±0.6 μmol/l after 4 weeks of insulin infusion and further reduced to 4.1±0.5 μmol/l after combined infusion of l-NAME and insulin. l-NAME treatment alone for 2 weeks in control rats significantly increased SBP by 33±2 mmHg (from 133±2 to 166±2 mmHg) and plasma insulin levels, as a consequence of insulin resistance. Despite marked increases in blood pressure due to infusion of insulin alone or in combination with l-NAME, the sodium balance, urinary sodium and water excretions, water intake and body weight gain of insulin/l-NAME-treated rats were not significantly different from rats without insulin infusion.ConclusionsSustained hyperinsulinemia causes partial impairment of NO production that may contribute to the development of insulin resistance and hypertension. Additional inhibition of NO synthesis by l-NAME accentuates the blood pressure elevation and insulin resistance in hyperinsulinemic rats. Furthermore, a rightward shift of the renal arterial pressure–natriuretic function relationship occurred in this hypertensive model.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID