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Hypertensive Status (hypertensive + status)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Pharmacogenetics of antihypertensive treatment

DRUG DEVELOPMENT RESEARCH, Issue 3 2004
Donna K. Arnett
Abstract Hypertension is a common disorder associated with increased cardiovascular morbidity and mortality. Unfortunately, in the United States, only about one third of those who are aware of their hypertensive status successfully control their blood pressure. One reason for this is the variable and unpredictable response individuals have to pharmacologic treatment. Clinicians often resort to a trial-and-error approach to match patients with effective drug treatment. It is the goal of hypertension pharmacogenetics to apply knowledge of genetic predictors of treatment response to drugs that lower blood pressure and to translate this knowledge into clinical practice. To date, more than 30 studies have investigated associations between specific genetic polymorphisms and response to particular antihypertensive drugs. Angiotensin-converting enzyme inhibitors have been most frequently studied, followed by diuretics, beta-blockers, angiotensin II blockers, adrenergic alpha-agonists, and calcium channel blockers. Renin,angiotensin,aldosterone system genes have been the most widely studied, with the angiotensin-converting enzyme I/D variant being typed in about one third of all hypertension pharmacogenetic studies to date. In a number of cases, significant and potentially promising associations between genes and drug treatments have been reported. However, taken in sum, the literature suggests that the path from gene-drug-outcome association studies to clinically useful knowledge may be neither short nor direct. In the future, carefully designed studies must acknowledge that hypertension is caused by multiple genes and environmental factors that act in concert. These considerations, along with a better understanding of the complexities of the biology of hypertension, open the next set of opportunities for hypertension pharmacogenetics research. Drug Dev. Res. 62:191,199, 2004. © 2004 Wiley-Liss, Inc. [source]

Differential regulation of the nitric oxide,cGMP pathway exacerbates postischaemic heart injury in stroke-prone hypertensive rats

EXPERIMENTAL PHYSIOLOGY, Issue 1 2007
Tetsuji Itoh
Using a working perfused heart model, we investigated the hypothesis that alterations in the NO,cGMP pathway may exacerbate postischaemic mechanical dysfunction in the hypertrophied heart. Ischaemia for 25 min followed by reperfusion for 30 min produced marked cardiac mechanical dysfunction in both stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY). Exogenous treatment with S -nitroso- N -acetyl- dl -penicillamine (SNAP), a NO donor, had beneficial effects on the cardiac dysfunction induced by ischaemia,reperfusion (I/R) in the WKY heart, but the cardioprotective effect of SNAP was eliminated by guanylyl cyclase inhibitor. Cardiac cGMP levels were increased by SNAP or ischaemia in WKY. In contrast, in SHRSP hearts, SNAP could not alleviate the cardiac dysfunction caused by I/R. Pre-ischaemia, the cardiac cGMP level was significantly higher in SHRSP than in WKY; however, no significant difference was found after SNAP and ischaemia. The myocardial Ca2+ -dependent NO synthase (NOS) activity increased at the end of ischaemia in WKY. Conversely, the Ca2+ -independent NOS activity and protein levels were upregulated by I/R in the SHRSP myocardium. In the SHRSP hearts, non-selective NOS and selective Ca2+ -independent NOS inhibitors or antioxidant treatment alleviated cardiac dysfunction caused by I/R. Moreover, mRNA expression and Western blotting analysis of cGMP-dependent protein kinase type I showed more deterioration of SHRSP hearts compared with WKY. These results suggest that: (1) the NO-dependent cardioprotective effect is depressed; and (2) overproduction of NO derived from Ca2+ -independent NOS contributes to postischaemic heart injury in the hypertrophied heart of hypertensive status. [source]

Parkinson's disease, stroke, and related epidemiology

MOVEMENT DISORDERS, Issue 11 2005
Andrew Nataraj MD
Abstract We investigated the prevalence of cerebrovascular disease and other comorbidities in Parkinson's disease (PD) patients compared to the general population. Five hundred PD patients were chosen randomly from one author's (A.H.R.) database. Age- and sex-matched controls were derived from 270 patients with essential tremor from the same database and from 490 patients in a general practitioner's database. Age, hypertensive status, smoking status, coronary artery disease, orthostatic hypotension, diabetes mellitus, and symptomatic cerebrovascular disease (stroke or transient ischemic attack) were assessed. Statistical analysis was performed using Pearson ,2 testing and binary logistic regression analysis. The prevalence of coronary artery disease, hypertension, diabetes mellitus, and orthostatic hypotension was similar among groups. The PD group had more patients who never smoked and less current smokers than the other groups. While there were similar frequencies of symptomatic cerebrovascular disease among groups, the prevalence of stroke was lower in PD patients. This difference disappeared upon stratification into groups based on smoking status and in the addition of smoking as a covariate in the multivariate analysis. Diminished smoking in PD patients likely plays a role in our finding of decreased stroke in patients with PD. Increased access to appropriate neurological care and subsequent prevention of stroke after a warning transient ischemic attack may also play a role, as may diminished levels of excitotoxic neurotransmitters in PD patients. © 2005 Movement Disorder Society [source]

Effect of quinapril on the attenuated heart rate recovery of type 2 diabetic subjects without known coronary artery disease

CLINICAL CARDIOLOGY, Issue 8 2004
Ilke Sipahi M.D.
Abstract Background: Heart rate (HR) recovery at 1 minis a measure of the vagal reactivation that occurs after cessation of exercise. Despite ample evidence about the association of attenuated HR recovery with increased mortality, pharmacologic modification of this predictor has not been shown. On the other hand, angiotensin-converting enzyme (ACE) inhibitors are known to have vagomimetic activity. Hypothesis: We hypothesized that ACE inhibition would increase HR recovery in a group of subjects known to have reduced HR recovery, namely diabetics. Methods: Maximal treadmill exercise stress test was performed in 31 type 2 diabetic and 31 nondiabetic male subjects with similar age, body mass index, and hypertensive status. None of the subjects had known heart disease or evidence of myocardial ischemia during the test. The diabetic subjects, after 2 weeks of treatment with quinapril, underwent a second exercise test. A third test was performed 2 to 3 weeks after cessation of quinapril treatment. Results: At baseline, despite similar exercise capacity, the diabetics had a lower HR recovery at 1 min than nondiabetics (25 ± 8 vs. 31 ± 8 beats/min, p<0.01). Quinapril significantly increased HR recovery at 1 min in diabetics (25 ± 8 beats/min at baseline vs. 28 ± 8 beats/min with quinapril vs. 25 ± 7 beats/min off-therapy, p < 0.01 by analysis of variance). Conclusions: The attenuated HR recovery of type 2 diabetics can be improved by quinapril. Whether the improvement in HR recovery with ACE inhibition can lead to decreased mortality is currently unknown. [source]