Essential Hypertension Part I: Definition and Etiology
TLDR
This review of current concepts regarding the definition, etiology, and treatment of essential hypertension is intended to aid the clinician in identifying those individuals at high risk who need to undergo evaluation and treatment, as well as in selecting optimal treatment strategies for hypertensive patients with comorbid conditions and/or target organ damage.Abstract:
Essential hypertension remains a major modifiable risk factor for cardiovascular disease (CVD) despite important advances in our understanding of its pathophysiology and the availability of effective treatment strategies. High blood pressure (BP) increases the risk of CVD for millions of people worldwide, and there is evidence that the problem is only getting worse. In the past decade, age-adjusted rates of stroke incidence have risen, and the slope of the age-adjusted rate of decline in coronary disease has leveled off. The incidence of end-stage renal disease and the prevalence of heart failure have also increased. A major contributor to these trends is inadequate control of BP in the hypertensive population. This review of current concepts regarding the definition, etiology, and treatment of essential hypertension is intended to aid the clinician in identifying those individuals at high risk who need to undergo evaluation and treatment, as well as in selecting optimal treatment strategies for hypertensive patients with comorbid conditions and/or target organ damage. The part of the review that deals with the genetic basis of hypertension and the gene/environment interaction that may lead to elevated BP is still a work in progress. Information gained from the Human Genome Project and from ongoing studies of the genetic basis of hypertension both in animal models and human populations may revolutionize the treatment of hypertension by replacing current empirical therapy with more effective, targeted treatments based on the genotype of the patient. Concepts introduced in this review form the basis for such “pharmacogenomic” approaches to antihypertensive therapy.
BP is a quantitative trait that is highly variable1 ; in population studies, BP has a normal distribution that is slightly skewed to the right. There is a strong positive and continuous correlation between BP and the risk of CVD (stroke, myocardial infarction, heart failure), renal disease, …read more
Citations
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Angiotensin-converting enzyme 2 is an essential regulator of heart function
Michael A. Crackower,Renu Sarao,Renu Sarao,Gavin Y. Oudit,Gavin Y. Oudit,Chana Yagil,Ivona Kozieradzki,Ivona Kozieradzki,Sam E. Scanga,Antonio J. Oliveira-dos-Santos,Joan da Costa,Liyong Zhang,York Pei,James W. Scholey,Carlos M. Ferrario,Armen S. Manoukian,Mark C. Chappell,Peter H. Backx,Peter H. Backx,Yoram Yagil,Josef M. Penninger +20 more
TL;DR: These genetic data for ACE2 show that it is an essential regulator of heart function in vivo and targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart.
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TL;DR: The novel concept that structural and functional abnormalities in the vasculature, including endothelial dysfunction, increased oxidative stress, vascular remodeling, and decreased compliance, may antedate hypertension and contribute to its pathogenesis has gained support in recent years.
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Pharmacological significance of triazole scaffold.
TL;DR: This paper is an attempt to review the pharmacological activities reported for triazole derivatives in the current literature with an update of recent research findings on this nuclei.
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Structure, endothelial function, cell growth, and inflammation in blood vessels of angiotensin II-infused rats: role of peroxisome proliferator-activated receptor-gamma.
Quy N. Diep,Mohammed El Mabrouk,Jeffrey S. Cohn,Dierk Endemann,Farhad Amiri,Agostino Virdis,Mario Fritsch Neves,Ernesto L. Schiffrin +7 more
TL;DR: Thiazolidinedione PPAR-&ggr; activators attenuated the development of hypertension, corrected structural abnormalities, normalized cell growth, and improved endothelial dysfunction induced by Ang II and prevented upregulation of angiotensin II type 1 receptors, cell cycle proteins, and proinflammatory mediators.
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Plasma β-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy
Mahmut Edip Gurol,Michael C. Irizarry,Eric E. Smith,S. Raju,Ramon Diaz-Arrastia,Teodoro Bottiglieri,J. Rosand,John H. Growdon,Steven M. Greenberg +8 more
TL;DR: Plasma β-amyloid 40 concentration is independently associated with extent of white matter hyperintensity in subjects with Alzheimer disease, mild cognitive impairment, or cerebral amyloid angiopathy, and if confirmed in longitudinal studies, these data would suggest circulating β-Amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly.
References
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The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure
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