摘要:

Hypertension and obesity are common medical conditions independently associated with increased cardiovascular risk. Many large epidemiological studies have demonstrated associations between body mass index and blood pressure, and there is evidence to suggest that obesity is a causal factor in the development of hypertension in obese individuals. Consequently, all hypertension management guidelines consider weight reduction as a first step in the management of increased blood pressure in obese individuals. Weight reduction may be achieved by behaviour modification, diet and exercise, or by the use of anti-obesity medications. However, the long-term outcomes of weight management programmes for obesity are generally poor, and most hypertensive patients will require antihypertensive drug treatment. Some classes of antihypertensive agents may have potentially unwanted effects on some of the metabolic and haemodynamic abnormalities that link obesity and hypertension, yet most hypertension guidelines fail to provide specific advice on the pharmacological management of obese patients. This may be because there are currently no studies examining the efficacy of specific antihypertensive agents in reducing mortality in obese hypertensive patients. This paper reviews the theoretical reasons for the differential use of the major classes of antihypertensive agents in the pharmacological management of obesity-related hypertension and also considers the potential role of anti-obesity agents.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo test the hypothesis that sleep-related breathing disorder (SRBD) is associated with increasing severity of cardiovascular risk markers.DesignA cross-sectional study of sleep laboratory patients.SettingUniversity Hospital Sleep Disorders Centre.PatientsWe studied 591 patients referred for a sleep study, all of them without a history of systemic hypertension.InterventionsClinical interview, two unattended sleep studies, and assessment of office blood pressure, cholesterol concentration, alcohol and nicotine consumption and daytime blood gases.Main outcome measurePost-hoc analysis of different cardiovascular risk markers: mean blood pressure, pulse pressure, and the type and grade of systemic hypertension.ResultsPatients were classified as normotensive (blood pressure<140/90 mmHg,n=228) or hypertensive (blood pressure⩾140/90 mmHg,n=363) according to office blood pressure measurements. Mixed (systolic and diastolic) hypertension was the most common type of hypertension (n=182), followed by isolated diastolic hypertension (n=101), borderline isolated systolic hypertension (n=70), and isolated systolic hypertension (n=10). The frequency of mixed hypertension increased with SRBD activity (P<0.05) and respiratory disturbance index (RDI; the number of breathing disorders per hour of estimated sleep time) was increased in those with mixed hypertension compared with those with normotension (24.8 compared with15.7;ttest:P<0.01). In hypertensive patients classified as having grades 1–3 of hypertension (n=265, 80 and 18, respectively), there was a progressive increase in RDI (18.9, 27.2 and 30.3, respectively,P<0.01). Mean blood pressure increased significantly with RDI. Pulse pressure increased significantly with age (P<0.001), but was unrelated to the degree of SRBD.ConclusionWe conclude that mean blood pressure and the severity of hypertension, but not pulse pressure, increase with the severity of the SRBD.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo examine the relationship between coronary (CHD) and cardiovascular (CVD) risk in patients with uncomplicated mild hypertension and to determine the accuracy of using CHD risk⩾15% over 10 years to identify for antihypertensive treatment those patients with CVD risk⩾20% over 10 years as advised in recent British guidelines.DesignComparison of decisions made using CHD risk⩾15% over 10 years calculated by the Framingham risk function and estimated using a simple table with CVD risk⩾20% over 10 years.SettingBritish population.SubjectsPeople aged 35–64 years with uncomplicated mild systolic hypertension (SBP 140–159 mmHg,n= 624) from the 1995 Scottish Health Survey.Main outcome measuresRelationship between CHD and CVD risk. Sensitivity, specificity, positive and negative predictive values (PPV and NPV).ResultsCHD risk 15% over 10 years was equivalent to CVD risk 21% over 10 years. Exact CHD risk⩾15% over 10 years had sensitivity 79%, specificity 98%, PPV 94% and NPV 93% in detecting CVD risk⩾20% over 10 years. Use of the table to estimate CHD risk⩾15% over 10 years gave sensitivity 88%, specificity 90%, PPV 76% and NPV 95%.ConclusionCHD risk appears acceptably accurate for targeting treatment in mild hypertension. The risk assessment table, which slightly overestimates CHD risk, was more sensitive in identifying patients with CVD risk⩾20% over 10 years and may be preferable to using exact CHD risk. European guidelines which suggest targeting treatment for mild hypertension at CHD risk⩾20% over 10 years are over-conservative compared with British guidelines.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveA significant inverse relationship between blood pressure and birth weight is firmly established. This association may be the result of fetal adaptations to an adverse intrauterine environment. Further markers of intrauterine growth include the weight of the placenta and the placental ratio (the ratio of placental weight to birth weight). A number of studies suggest that a decreased placental weight or an elevated placental ratio may be independent risk factors for subsequent high blood pressure. The overall evidence for this is, however, inconclusive. The purpose of the present study was to clearly define the relationships between placental weight, placental ratio and subsequent blood pressure during childhood.DesignProspective cohort study of 2507 singleton children, born at term during 1989–1992. Blood pressures were recorded at ages 1, 3 and 6 years, using a semi-automated oscillometric device.ResultsInverse relationships existed between both systolic and diastolic blood pressure and placental weight, adjusted for current weight at ages 1, 3 and 6 years. The relationships between placental weight and systolic blood pressure were statistically significant at ages 1 and 3 years. There was no consistent relationship between placental weight and later blood pressure within birth weight categories. No clinically or statistically significant association was seen between the placental ratio and either systolic or diastolic blood pressures at any age.ConclusionsBirth weight, rather than placental weight or their ratio, is the early life factor most importantly related to subsequent blood pressure in childhood.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

BackgroundIt has recently been demonstrated that the smoothness index (SI) (the ratio between the average of the blood pressure changes computed for each hour of the recording and its standard deviation), a new and reproducible measure of the homogeneity of blood pressure reduction by antihypertensive treatment, has evident advantages over trough-to-peak ratio (T/P) in the prediction of the regression of left ventricular hypertrophy. Therefore we considered it to be worthwhile to compare the ability of SI and T/P to predict changes of the carotid artery intima–media thickness (IMT) during pharmacological treatment in patients with essential hypertension.MethodsIn 100 patients with essential hypertension, 24 h ambulatory blood pressure and carotid artery IMT were measured after 3 weeks of therapeutic wash-out and after 12 months of antihypertensive treatment (calcium antagonists, diuretics, angiotensin converting enzyme (ACE) inhibitors or β-blockers). The homogeneity of the effect of treatment over blood pressure was evaluated by computing T/P and SI.ResultsTwenty-four hour blood pressure was significantly reduced by therapy, while, on average, a small but significant increase in indices of carotid artery wall thickness was observed. However, IMT was clearly reduced in patients with high SI. Statistically significant correlations were observed between changes in indices of carotid artery IMT during therapy and SI. No significant correlation was observed between indices of carotid artery morphology and T/P, basal 24 h blood pressure or changes in blood pressure during therapy.ConclusionsSI, but not T/P is the predictor of changes in carotid artery wall thickness. The information provided by SI is independent from basal blood pressure values. For carotid artery morphology, the smoothness of blood pressure reduction is even more important than its absolute change.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Objectives and methods:Oral contraceptives (OC) usage increases serum angiotensinogen levels to three to five times normal and about 5% of these women develop arterial hypertension. The genetic contribution to this susceptibility to OC-induced hypertension is poorly understood. We have analyzed the genotypes of 149 hypertensive and 101 normotensive women using oral contraceptives, for three genetic polymorphisms in genes of the renin–angiotensin system: an insertion/deletion (I/D) in the angiotensin converting enzyme (ACE) gene, the T235M polymorphism of the angiotensinogen gene (AGT) and a point mutation in its promoter.ResultsAfter cessation of oral contraception the mean arterial pressures of the hypertensive women were separable into two non-overlapping groups; 88 of the women remained hypertensive and 61 returned to normal blood pressure. Both groups of hypertensive women had a similarly higher frequency of hypertensive relatives than the normotensive women, but were otherwise similar. The 235T allele of AGT was significantly increased in frequency in the 61 oral contraceptive-inducible hypertensive women compared with the controls and the 88 women that remained hypertensive. The ACE I/D genotypes were similarly distributed within the three groups of women, but were distinctly non-random in the oral contraceptive-induced hypertensive women when they were also classified by AGT genotype.Conclusion:This statistical interaction of genotype frequencies suggests that the genetic basis of susceptibility to OC-induced hypertension is complex.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ObjectiveTo test the hypothesis that the Ca2+signal transduction process in endothelial cells from genetically hypertensive rats (SHR) is affected by an overproduction of free radicals.MethodsThe Ca2+response to the inositol 1,4,5-triphosphate (IP3) mobilizing agonist, ATP, was measured using the fluorescent probe, fura-2, in endothelial cells from Sprague–Dawley rats, and in young and age-matched genetically hypertensive rats (SHR). The effect of free radicals and reducing agents on the intracellular release of Ca2+and IP3production was determined in resting and ATP-stimulated cells. Experiments were also performed to compare the level of expression and enzymatic activity of catalase and superoxide dismutase (SOD ) in endothelial cells from SHR and Sprague–Dawley rats.ResultsThe exposure of aortic endothelial cells from Sprague–Dawley rats to the free-radical generating system, hypoxanthine + xanthine oxidase (HX/XO), caused a time- and concentration-dependent inhibition of the ATP-induced Ca2+response. A similar HX/XO-dependent inhibition was also observed in Sprague–Dawley cells stimulated with the endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin. Incubation with the antioxidative enzymes, catalase and SOD, had no effect on the ATP-induced Ca2+release in Sprague–Dawley cells, but led to a strong increase in the internal release of Ca2+in cells from adult (12 weeks old) or young (3 weeks old) SHR. The effect of antioxidants was not related either to an enhancement of the ATP-induced production of IP3, or to a lower expression and activity of SOD and catalase.ConclusionThe present work provides evidence that the Ca2+signalling process in SHR endothelial cells is affected by an overproduction of free radicals, resulting in a depletion of releasable Ca2+from IP3-sensitive and -insensitive Ca2+pools. These results point towards a beneficial action of antioxidants on Ca2+signalling in endothelial cells from models of hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

BackgroundVascular smooth muscle cell (VSMC) proliferation induced by various growth factors has been implicated in a wide variety of pathological processes, including hypertension, atherosclerosis and restenosis after angioplasty.ObjectivesTo investigate the interactions among well-known potent vasoconstrictor substances, endothelin-1 (ET-1), angiotensin II (Ang II), and serotonin (5-HT), on VSMC proliferation.MethodsGrowth-arrested rabbit VSMCs were incubated with different concentrations of ET-1 in the absence or presence of Ang II, 5-HT, or both. VSMC proliferation was examined by increases in incorporation of [3H]thymidine into DNA and in cell number.ResultsET-1, Ang II and 5-HT stimulated DNA synthesis in a dose-dependent manner. ET-1 had a maximal effect at a concentration of 0.5 μmol/l (259% of control), Ang II at 1 μmol/l (173%), and 5-HT at 50 μmol/l (205%). When added together, ET-1 (0.1 μmol/l) and Ang II (1 μmol/l) synergistically induced DNA synthesis (341%). When the vasoconstrictors were tested in combination, even non-mitogenic concentrations of ET-1 (0.01 nmol/l) potentiated 5-HT (5 μmol/l)-induced DNA synthesis (404%). Co-incubation of ET-1 (0.01 μmol/l) with Ang II (1 μmol/l) and 5-HT (5 μmol/l) synergistically induced DNA synthesis (566%). These effects on DNA synthesis were paralleled by an increase in cell number. The ETA/Bnon-selective receptor antagonist, TAK044 (1 μmol/l) and the ETAreceptor antagonist, BQ123 (1 μmol/l), but not the ETBreceptor antagonist, BQ788 (1 μmol/l), inhibited the mitogenic effect of ET-1 and its interaction with Ang II or 5-HT. In addition, TAK044 (1 μmol/l) or BQ123 (1 μmol/l) along with the angiotensin II type 1 (AT1) receptor antagonist, candesartan (1 μmol/l), the 5-HT2Areceptor antagonist, sarpogrelate (10 μmol/l), or both, inhibited the interactions of ET-1 with Ang II or 5-HT.ConclusionsOur results suggest that Ang II and 5-HT could potentiate ET-1-induced VSMC proliferation. Inhibition of ETA, AT1, and 5-HT2Amay be effective in the treatment of VSMC proliferative disorders associated with hypertension, atherosclerosis and restenosis after angioplasty.

ISSN:0263-6352    

出版商:OVID    

年代:2001

数据来源: OVID