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      Why do hypertensive patients of African ancestry respond better to calciumblockers and diuretics than to ACE inhibitors and β-adrenergic blockers? Asystematic review

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      BMC Medicine
      Springer Science and Business Media LLC

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          Abstract

          Background Clinicians are encouraged to take an individualized approach when treating hypertension in patients of African ancestry, but little is known about why the individual patient may respond well to calcium blockers and diuretics, but generally has an attenuated response to drugs inhibiting the renin-angiotensin system and to β-adrenergic blockers. Therefore, we systematically reviewed the factors associated with the differential drug response of patients of African ancestry to antihypertensive drug therapy. Methods Using the methodology of the systematic reviews narrative synthesis approach, we sought for published or unpublished studies that could explain the differential clinical efficacy of antihypertensive drugs in patients of African ancestry. PUBMED, EMBASE, LILACS, African Index Medicus and the Food and Drug Administration and European Medicines Agency databases were searched without language restriction from their inception through June 2012. Results We retrieved 3,763 papers, and included 72 reports that mainly considered the 4 major classes of antihypertensive drugs, calcium blockers, diuretics, drugs that interfere with the renin-angiotensin system and β-adrenergic blockers. Pharmacokinetics, plasma renin and genetic polymorphisms did not well predict the response of patients of African ancestry to antihypertensive drugs. An emerging view that low nitric oxide and high creatine kinase may explain individual responses to antihypertensive drugs unites previous observations, but currently clinical data are very limited. Conclusion Available data are inconclusive regarding why patients of African ancestry display the typical response to antihypertensive drugs. In lieu of biochemical or pharmacogenomic parameters, self-defined African ancestry seems the best available predictor of individual responses to antihypertensive drugs.

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          Most cited references121

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          Arginine metabolism: nitric oxide and beyond.

          Arginine is one of the most versatile amino acids in animal cells, serving as a precursor for the synthesis not only of proteins but also of nitric oxide, urea, polyamines, proline, glutamate, creatine and agmatine. Of the enzymes that catalyse rate-controlling steps in arginine synthesis and catabolism, argininosuccinate synthase, the two arginase isoenzymes, the three nitric oxide synthase isoenzymes and arginine decarboxylase have been recognized in recent years as key factors in regulating newly identified aspects of arginine metabolism. In particular, changes in the activities of argininosuccinate synthase, the arginases, the inducible isoenzyme of nitric oxide synthase and also cationic amino acid transporters play major roles in determining the metabolic fates of arginine in health and disease, and recent studies have identified complex patterns of interaction among these enzymes. There is growing interest in the potential roles of the arginase isoenzymes as regulators of the synthesis of nitric oxide, polyamines, proline and glutamate. Physiological roles and relationships between the pathways of arginine synthesis and catabolism in vivo are complex and difficult to analyse, owing to compartmentalized expression of various enzymes at both organ (e.g. liver, small intestine and kidney) and subcellular (cytosol and mitochondria) levels, as well as to changes in expression during development and in response to diet, hormones and cytokines. The ongoing development of new cell lines and animal models using cDNA clones and genes for key arginine metabolic enzymes will provide new approaches more clearly elucidating the physiological roles of these enzymes.
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            Hypertension in sub-Saharan African populations.

            Hypertension in sub-Saharan Africa is a widespread problem of immense economic importance because of its high prevalence in urban areas, its frequent underdiagnosis, and the severity of its complications. We searched PubMed and relevant journals for words in the title of this article. Among the major problems in making headway toward better detection and treatment are the limited resources of many African countries. Relatively recent environmental changes seem to be adverse. Mass migration from rural to periurban and urban areas probably accounts, at least in part, for the high incidence of hypertension in urban black Africans. In the remaining semirural areas, inroads in lifestyle changes associated with "civilization" may explain the apparently rising prevalence of hypertension. Overall, significant segments of the African population are still afflicted by severe poverty, famine, and civil strife, making the overall prevalence of hypertension difficult to determine. Black South Africans have a stroke rate twice as high as that of whites. Two lifestyle changes that are feasible and should help to stem the epidemic of hypertension in Africa are a decreased salt intake and decreased obesity, especially in women. Overall, differences from whites in etiology and therapeutic responses in sub-Saharan African populations are graded and overlapping rather than absolute. Further studies are needed on black Africans, who may (or may not) be genetically and environmentally different from black Americans and from each other in different parts of this vast continent.
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              Testing Methodological Guidance on the Conduct of Narrative Synthesis in Systematic Reviews: Effectiveness of Interventions to Promote Smoke Alarm Ownership and Function

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                Author and article information

                Journal
                BMC Medicine
                BMC Med
                Springer Science and Business Media LLC
                1741-7015
                December 2013
                May 30 2013
                December 2013
                : 11
                : 1
                Article
                10.1186/1741-7015-11-141
                c9344679-a1f9-41f8-b4cb-f75973ac9c58
                © 2013

                http://www.springer.com/tdm

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