ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectiveTo review the current literature on sympathetic mediation of hypertension in chronic renal failure.BackgroundHypertension is present in the vast majority of patients with chronic renal failure and constitutes a major risk factor for the excessive cardiovascular morbidity and mortality in this patient population. Although, traditionally, this hypertension is thought to be largely volume-dependent, an increasing body of literature suggests that there is an important sympathetic neural component. Microneurographic studies have demonstrated sympathetic overactivity without baroreflex impairment in both hypertensive chronic hemodialysis patients as well as in those with less advanced renal insufficiency. Sympathetic nerve activity was found to be normal in hemodialysis patients with bilateral nephrectomy, leading to the hypothesis that sympathetic overactivity in uremia is caused by a neurogenic signal (carried by renal afferents) arising in the failing kidney. This hypothesis is supported by rat studies showing that renal deafferentation abrogates hypertension in the 5/6 nephrectomy model of chronic renal insufficiency. In addition, in patients with chronic renal insufficiency and renin-dependent hypertension, sympathetic overactivity was normalized by chronic angiotensin converting enzyme inhibition but not by calcium channel blockade, implicating a major central neural action of angiotensin II.ConclusionsSympathetic overactivity in chronic renal failure is caused by neurohormonal mechanisms arising in the failing kidney. Future clinical studies are needed to determine whether normalization of sympathetic activity should constitute an important therapeutic goal in this high-risk patient population.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10% of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin–angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes ‘autonomous’ and hence ‘tertiary’ aldosteronism in a significant proportion of hypertensives.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectiveTo examine the relation of anger expression with blood pressure and hypertension among Japanese.DesignA cross-sectional study.MethodsSubjects were 4374 men and women aged 30–74 years from rural and urban communities. Anger expression was estimated using the anger-out and anger-in scores of the Spielberger Anger Expression Scale. Multiple linear regression analyses were performed to estimate the associations of anger expression scores with blood pressure. Proportions of hypertensives among the tertiles of anger expression scores and the relative odds of hypertension for low versus high tertiles of anger expression scales were calculated using logistic regression models.ResultsThe anger-out score was inversely associated with systolic and diastolic blood pressure levels for men; a four-point (one standard deviation) lower anger-out score was associated with 1.6 mmHg [95% confidence interval (CI), 0.6–2.6] greater systolic blood pressure and 0.6 mmHg (95% CI, −0.03 to 1.2) greater diastolic pressure after adjustment for age, body mass index, alcohol intake, smoking category, and parental history of hypertension. The adjusted relative odds of hypertension for low versus high tertiles of anger-out was 1.60 (95% CI, 1.19–2.15). These inverse associations were more evident among men with low coping behavior than among those with high coping behavior. For women, the anger-out score was not associated with blood pressure. There was no relation between the anger-in score and either blood pressure or hypertension in either men or women.ConclusionsThis study suggests that Japanese men who do not express their anger, especially when they have low coping behavior, may have an increased risk of high blood pressure.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

BackgroundTreating hypertension with drugs is so far the most cost-effective way to reduce this important risk factor for cardiovascular disease (CVD). It is, however, important to determine absolute risk, and thereby estimate indication for drug treatment, in order to maintain a cost-effective drug treatment. WHO/ISH Hypertension Guidelines from 1999 propose a risk stratification for estimating absolute risk for CVD based on blood pressure and additional risk factors, target organ damage (TOD) and CVD.ObjectivesWe studied the consequences of applying the recent WHO/ISH risk stratification scheme to a MONICA sample of 6000 subjects from a geographically defined population in northern Sweden, regarding indications for treatment, target blood pressure and risk distribution.MethodsWe have risk-classified each of these patients using a computer program, according to the WHO/ISH scheme. Data on TOD were not available.ResultsIn all, 917 (15%) had drug-treated hypertension. Three-quarters (n= 737) were inadequately treated, with blood pressure levels at or above 140 or 90 mmHg. 1773 (30% of 5997) untreated subjects had a blood pressure of 140/90 or above; 16% in the low-, 62% in the medium-, 8% in the high-, and 14% in the very-high-risk group. The corresponding risk-group pattern for the inadequately treated hypertensives (n= 737) was 5.5, 48.3, 11.1 and 35.2%, respectively. If we shifted the target blood pressure from below 140/90 to below 130/85 for drug-treated subjects under 60 (n= 278) the number of inadequately treated subjects increased by 34 (12.2% of 278); 14 in the low-risk group, 15 in the medium-risk group, and only five in the high- or very-high-risk groups.ConclusionsOnly one-fifth of the drug-treated hypertensives were well controlled. Moreover, the incidence of newly detected blood pressure elevation was high. The majority of younger subjects with high blood pressure had low risk, but in those aged 45–54 this had already risen to a medium risk. Changing the target blood pressure to below 130/85, for subjects aged below 60, as recommended by WHO/ISH, affects predominantly low- and medium-risk groups.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectiveAn increased frequency of the angiotensin converting enzyme (ACE) D variant has recently been reported in patients with atheromatous renal artery disease (RAD), whereas controversy exists on the risk of coronary artery disease (CAD) associated with this polymorphism. In spite of the frequent coexistence of RAD and CAD, no studies have specifically compared ACE insertion/deletion (I/D) polymorphism in patients with coronary versus renal artery disease or defined the risk of each disease associated with the D variant.DesignWe designed a large case–control study of subjects for whom objective renal or coronary angiographic documentation was available.Methods and resultsWe analysed ACE I/D genotype and clinical–biochemical data of a total of 942 subjects (123 patients with and 137 without angiographic evidence of RAD, 420 patients with and 262 without angiographic evidence of CAD). Renal (with and without RAD) and coronary patients were similar for most conventional risk factors. There was no difference inDDfrequency between CAD and CAD-free patients (38.1 versus 33.6%, NS) andDDhomozygosity was not associated with CAD risk (OR = 1.27, 95% CI = 0.82–1.98). In contrast, theDDgenotype was more frequent in RAD than in RAD-free patients (54.5 versus 39.4,P<0.05) and was associated with a 2.25-fold increased risk of RAD in both the univariate and multivariate logistic regression models. Additional predictors of RAD were age and creatinine. In RAD/RAD-free patients with angiographically documented CAD,DDhomozygosity was confirmed to be preferentially associated with RAD (P<0.05).ConclusionsACE D variant is preferentially associated with atherosclerotic renal rather than with coronary disease, despite similar exposure to atherogenic noxae.DDhomozygosity confers a 2.25-fold increased risk of RAD.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectiveTo localize quantitative trait loci (QTL) in an animal model that is potentially relevant to human hypertension.Design and methodsFour congenic strains have been constructed by replacing various segments of the Dahl salt-sensitive (S) rat by those of the Lewis (LEW) rat. A marker-assisted approach was employed to facilitate this process. When these congenic strains were established, their blood pressures (BPs) were measured by telemetry and compared with that of the S rat. Moreover, a search was conducted to find possible intermediate phenotypes linking the BP effects of the QTL and other physiological traits.ResultsTwo BP QTL, designated as QTL1 and QTL2, have been mapped to the regions of 4.2 centiMorgans (cM) and less than 12.1 cM respectively on rat chromosome 10. The effects of both QTL correlate with cardiac, left ventricular and aortic hypertrophy. The effect of QTL1 is also associated with renal hypertrophy.ConclusionThe current study proved that multiple QTL exist in the region of Dahl rat chromosome 10. The identification of these QTL may help unravel the mechanisms underlying the pathogenesis of certain QTL in humans.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectivesWe investigated the influence of hyperhomocysteinemia and high salt intake on sodium handling, oxidative state, vascular endothelial function and blood pressure in a rat model.MethodsEight-week-old male Sprague–Dawley rats were divided into subgroups and maintained for 4 weeks prior to experimentation on either control chow containing 0.36% methionine and 0.5% NaCl; or one of the following modified diets containing either 0.7% methionine, 8% NaCl or 0.7% methionine + 8% NaCl. Sodium handling, homocysteine metabolism, lipid profile, NO synthesis, oxidative state, blood pressure and relaxation to acetylcholine of carotid rings were evaluated and compared.ResultsDiet-induced mild hyperhomocysteinemia (plasma homocysteine levels 1.4-fold higher than control), by itself, had no significant influence on sodium excretion, vascular endothelial function and blood pressure. Increased salt intake had no influence on homocysteine metabolism, vascular endothelial function and blood pressure. The coexistence of mild hyperhomocysteinemia and high salt intake significantly diminished vascular endothelial function (rmaxto acetylcholine; control chow 83.2±6.2%, 0.7% methionine diet 74.7±3.9%, 8% NaCl diet 85.1±4.6%, 0.7% methionine + 8% NaCl diet 57.9±6.6%) but manifested no rise in blood pressure. No significant difference in oxidative state was observed in this analysis.ConclusionsDiet-induced mild hyperhomocysteinemia, the extent of which is comparable with the levels that are associated with a predisposition to common atherosclerotic diseases, was found to induce vascular endothelial dysfunction only when accompanied by high salt intake.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

ObjectiveBiosynthesis of eicosanoid metabolites in blood vessels regulates vascular tone and platelet function. We investigated whether intraluminal pressure modulates gene and protein expression of key eicosanoid enzymes in intact human conduit vessels and/or release of their vasoactive metabolites.MethodsPaired segments of human umbilical veins were perfused under laminar flow for 1.5, 3 and 6 h at high versus low intraluminal pressure (40/20 mmHg) with identical shear stress (10 dyn/cm2). Endothelial cell mRNAs encoding cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), prostaglandin synthase (PGS), and thromboxane synthase (TXS) were measured by quantitative real-time RT-PCR. Secretion of PGI2and TXA2to the perfusion medium was measured by enzyme immunoassay of their metabolites 6-keto-prostaglandin F1βand TXB2.ResultsIntraluminal pressures were 39.9±0.02 and 20.0±0.03 mmHg (P<0.0001) in high and low pressure circuits, and shear stress levels were 10.6±0.60 and 9.7±0.36 dyn/cm2(NS, not significant). COX-1 mRNA was significantly up-regulated after 1.5 h of high pressure stimulation and continued up to 3 h, but fell thereafter significantly below baseline after 6 h. COX-2 mRNA was initially significantly down-regulated, followed by a significant up-regulation after 6 h. Gene expressions of PGS and TXS were significantly induced after 6 h of high pressure perfusion. High pressure depressed the production of PGI2(P<0.05) but did not alter TXA2formation.ConclusionsIntraluminal pressure has differential effects on gene and protein expression of key eicosanoid enzymes and biosynthesis of prostanoid metabolites in intact human conduit vessles. The new, computerized biomechanical perfusion system may be a useful tool to elucidate specific effects of various biomechanical forces on intact mammalian conduit vessels.

ISSN:0263-6352    

出版商:OVID    

年代:2002

数据来源: OVID