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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.ashjournal.com/?rss=yes"><title>Journal of the American Society of Hypertension</title><description>Journal of the American Society of Hypertension RSS feed: Current Issue.    The  Journal of the American Society of Hypertension (JASH)  publishes peer-reviewed articles on the topics of basic, applied 
and translational research on blood pressure, hypertension and related cardiovascular disorders and factors. Original research studies, 
reviews, hypotheses, editorial commentary and special reports spanning the spectrum of human and experimental animal and tissue research 
will be considered. All research studies must have been conducted following animal welfare guidelines.  Studies involving human subjects 
or tissues must have received approval of the appropriate institutional committee charged with oversight of human studies and informed 
consent must be obtained. 
 
This  Journal  is covered in MEDLINE, Chemical Abstracts Service, EMBASE, and Scopus.   </description><link>http://www.ashjournal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 American Society of Hypertension. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:issn>1933-1711</prism:issn><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2012</prism:publicationDate><prism:copyright> © 2012 American Society of Hypertension. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS193317111100283X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002385/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002427/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002063/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002452/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002464/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002415/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002373/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002403/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002907/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171111002919/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.ashjournal.com/article/PIIS193317111100283X/abstract?rss=yes"><title>From the Editor</title><link>http://www.ashjournal.com/article/PIIS193317111100283X/abstract?rss=yes</link><description>This issue begins with three review articles. The first, by Drs. Rosenthal and Alter, is an extensive review of a much-neglected issue often related to hypertension: that of occupational stress. Perusal of this review should provide many new insights into this area and suggestions for further investigation. Dr. Friedrich Luft, Deputy Editor of JASH, follows with a review of a provocative paper recently presented at the American Heart Association Council for High Blood Pressure Research. This study suggests that immunosuppression may modify the effect of blood pressure on end-organ function. The third review, by Drs. Feldstein and Weder, addresses another often-ignored issue in hypertension: that of orthostatic hypotension in hospitalized patients. Not only is this a frequent cause of falls in the older subject, but careful measurement of supine, followed by upright, blood pressure before hospital discharge (and indeed in every encounter with treated hypertensive patients) should provide increased recognition of this common problem.</description><dc:title>From the Editor</dc:title><dc:creator>Myron H. Weinberger</dc:creator><dc:identifier>10.1016/j.jash.2011.11.002</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>1</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002385/abstract?rss=yes"><title>Occupational stress and hypertension</title><link>http://www.ashjournal.com/article/PIIS1933171111002385/abstract?rss=yes</link><description>Abstract: Occupational stress, or job strain, resulting from a lack of balance between job demands and job control, is considered one of the frequent factors in the etiology of hypertension in modern society. Stress, with its multifactorial causes, is complex and difficult to analyze at the physiological and psychosocial levels. The possible relation between job strain and blood pressure levels has been extensively studied, but the literature is replete with conflicting results regarding the relationship between the two. Further analysis of this relationship, including the many facets of job strain, may lead to operative proposals at the individual and public health levels designed to reduce the effects on health and well-being. In this article, we review the literature on the subject, discussing the various methodologies, confounding variables, and suggested approaches for a healthier work environment.</description><dc:title>Occupational stress and hypertension</dc:title><dc:creator>Talma Rosenthal, Ariela Alter</dc:creator><dc:identifier>10.1016/j.jash.2011.09.002</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>2</prism:startingPage><prism:endingPage>22</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002427/abstract?rss=yes"><title>Neural regulation of the immune system modulates hypertension-induced target-organ damage</title><link>http://www.ashjournal.com/article/PIIS1933171111002427/abstract?rss=yes</link><description>Abstract: Innate and acquired immune mechanisms are involved in hypertension-induced target-organ damage. Immunosuppressive treatments directed at T lymphocytes, NF-κB activation, or tumor necrosis factor-alpha production are all successful in ameliorating cardiac or renal injury. Recently, important modulatory functions involving the autonomic nervous system have been uncovered. Involved are an afferent detection arm that sends vagal-mediated signals to the brain and an efferent arm that includes the spleen and important nicotinic acetylcholine receptor subunit. The signaling attenuates inflammatory activity. Splenectomy or operations that injure the vagus or splenic abrogate these important protective mechanisms. Vagal stimulation, either electrical or pharmacological, could provide additional protection. The field of neuroimmunology will become increasingly important to cardiovascular clinicians.</description><dc:title>Neural regulation of the immune system modulates hypertension-induced target-organ damage</dc:title><dc:creator>Friedrich C. Luft</dc:creator><dc:identifier>10.1016/j.jash.2011.09.006</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-11-03</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-11-03</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>23</prism:startingPage><prism:endingPage>26</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002063/abstract?rss=yes"><title>Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients</title><link>http://www.ashjournal.com/article/PIIS1933171111002063/abstract?rss=yes</link><description>Abstract: Orthostatic hypotension (OH) is strongly age-dependent, with a prevalence ranging from 5% to 11% in middle age to 30% or higher in the elderly. It is also closely associated with other common chronic diseases, including hypertension, congestive heart failure, diabetes mellitus, and Parkinson’s disease. Most studies of OH have been performed in population cohorts or elderly residents of extended care facilities, but in this review, we draw attention to a problem little studied to date: OH in hospitalized patients. The prevalence of OH in all hospitalized patients is not known because most studies have included only older individuals with multiple comorbid diseases, but in some settings as many as 60% of hospitalized adults have postural hypotension. Hospitalized patients are particularly vulnerable to the consequences of OH, particularly falls, because postural blood pressure (BP) regulation may be disturbed by many common acute illnesses as well as by bed rest and drug treatment. The temporal course of OH in hospitalized patients is uncertain, both because the reproducibility of OH is poor and because conditions affecting postural BP regulation may vary during hospitalization. Finally, OH during hospitalization often persists after discharge, where, in addition to creating an ongoing risk of falls and syncope, it is strongly associated with risk of incident cardiovascular complications, including myocardial infarction, heart failure, stroke, and all-cause mortality. Because OH is a common, easily diagnosable, remediable condition with important clinical implications, we encourage caregivers to monitor postural BP change in patients throughout hospitalization.</description><dc:title>Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients</dc:title><dc:creator>Carlos Feldstein, Alan B. Weder</dc:creator><dc:identifier>10.1016/j.jash.2011.08.008</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-11-18</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-11-18</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>27</prism:startingPage><prism:endingPage>39</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002452/abstract?rss=yes"><title>Autoantibody activation of beta-adrenergic and muscarinic receptors contributes to an “autoimmune” orthostatic hypotension</title><link>http://www.ashjournal.com/article/PIIS1933171111002452/abstract?rss=yes</link><description>Abstract: Background: Orthostatic hypotension (OH) is characterized by an abnormal autonomic response to upright posture. Activating autoantibodies to β1/2-adrenergic (AAβ1/2AR) and M2/3 muscarinic receptors (AAM2/3R) produce vasodilative changes in the vasculature that may contribute to OH.Methods: Immunoglobulin (Ig)G from 6 patients with idiopathic OH harboring autoantibodies and from 10 healthy control subjects were examined for: 1) β1AR and M2R activity with a perfused Purkinje fiber assay and PKA assay in H9c2 cells and 2) vasodilator β2AR and M3R activity using a pressurized cremaster resistance arteriole assay. Changes in IgG activity with and without propranolol, atropine, and L-NAME were used to estimate AAβAR, AAM2R, and AAM3R activation of their respective functions.Results: All six patients had elevated enzyme-linked immunosorbent assay titers to at least one of the receptors compared with controls. βAR-mediated contractility activity and M2R activity were increased in five of the six patients. IgG from all six patients produced a direct vasodilator effect on cremaster arterioles. βAR and nitric oxide synthase blockade led to near normalization of IgG-induced vasodilation.Conclusion: AAβ1/2AR and AAM2/3R are present in some patients with idiopathic OH compatible with an in vivo effect. These autoantibodies and their cardiovascular effects provide new mechanistic insights into the pathophysiology of OH.</description><dc:title>Autoantibody activation of beta-adrenergic and muscarinic receptors contributes to an “autoimmune” orthostatic hypotension</dc:title><dc:creator>Xichun Yu, Stavros Stavrakis, Michael A. Hill, Shijun Huang, Sean Reim, Hongliang Li, Muneer Khan, Sean Hamlett, Madeleine W. Cunningham, David C. Kem</dc:creator><dc:identifier>10.1016/j.jash.2011.10.003</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>40</prism:startingPage><prism:endingPage>47</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002464/abstract?rss=yes"><title>Correlation of arterial blood pressure and compliance with left ventricular structure and function in the very elderly</title><link>http://www.ashjournal.com/article/PIIS1933171111002464/abstract?rss=yes</link><description>Abstract: There are very few data on the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), arterial compliance, and left ventricular structure and function, particularly left ventricular hypertrophy (LVH), in the very elderly (&gt;75 years). SBP and arterial stiffness increase with age, and the question is: which of the two is the main stimulus to LVH? This is a cross-sectional study to compare blood pressure and arterial stiffness measures with regard to their correlations with echocardiographic parameters of LV structure and function, controlling for age and cardiovascular risk factors, in a very elderly population. Arterial stiffness was determined by radial pulse waveform using pulse contour analysis. LV dimensions were measured by transthoracic M-mode echocardiography, and diastolic function by tissue Doppler measurements of diastolic mitral annular velocities. There were 179 subjects, all male, with a mean age of 81.8 years. Using age-adjusted partial correlations, SBP, DBP, and mean arterial pressure (MAP) were correlated with parameters of LV structure and function. Correlation coefficients were: SBP versus left ventricular mass index (LVMI), r = 0.246; SBP versus early diastolic mitral annular velocity (MAV), r = −0.179; DBP versus LVMI, r = 0.199; DBP versus MAV, r = −0.199; MAP versus LVMI, r = 0.276; and MAP versus MAV, r = −0.206, all with P &lt; .05. However, neither capacitative nor reflective arterial compliance was significantly correlated with any parameter of LV structure and function. After controlling for age and 10 cardiovascular and metabolic risk factors, the correlation between blood pressure and the measured LV parameters was substantially unchanged, as was the lack of correlation between indices of arterial compliance and the LV indices. Arterial blood pressure is correlated with LV structure and function in the very elderly, but arterial stiffness, as measured by diastolic pulse contour analysis, is not.</description><dc:title>Correlation of arterial blood pressure and compliance with left ventricular structure and function in the very elderly</dc:title><dc:creator>Clive Rosendorff, Orson Go, James Schmeidler, Jeremy M. Silverman, Michal S. Beeri</dc:creator><dc:identifier>10.1016/j.jash.2011.10.004</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>48</prism:startingPage><prism:endingPage>55</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002415/abstract?rss=yes"><title>Aldosterone and aldosterone: renin ratio associations with insulin resistance and blood pressure in African Americans</title><link>http://www.ashjournal.com/article/PIIS1933171111002415/abstract?rss=yes</link><description>Abstract: African Americans have more hypertension and hypertension-related morbidity than whites. Aldosterone, in presence of a high salt intake, contributes to hypertension and tissue injury. Inappropriately elevated aldosterone levels could explain this racial disparity. Our study was conducted to determine if aldosterone is associated with elevated blood pressure (BP) or insulin resistance, independent of obesity. A study was conducted on 483 young adult African Americans without cardiovascular or renal disease. Measurements included anthropometrics, BP, lipids, glucose, insulin, aldosterone, and renin. Urine sodium and potassium estimated sodium intake. The cohort was stratified by tertiles of aldosterone and tertiles of aldosterone/renin ratio (ARR). Average urine sodium/potassium ratio was &gt;3.0 in all groups. Insulin resistance, estimated by homeostasis model, was lowest in the low aldosterone group (geometric mean 1.5 [0.6, 2.2]) compared with the high aldosterone group (1.7 [0.9, 2.7], P &lt; .01). Adjusted analyses detected a significant association of aldosterone with insulin resistance, independent of other variables. BP was significantly higher in the high ARR group compared with low and mid ARR groups (P &lt; .01). The significant association of ARR with BP with high dietary sodium suggests that insufficiently suppressed aldosterone may contribute to BP sensitivity to sodium in African Americans.</description><dc:title>Aldosterone and aldosterone: renin ratio associations with insulin resistance and blood pressure in African Americans</dc:title><dc:creator>Yonghong Huan, Stephanie DeLoach, Scott W. Keith, Theodore L. Goodfriend, Bonita Falkner</dc:creator><dc:identifier>10.1016/j.jash.2011.09.005</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>56</prism:startingPage><prism:endingPage>65</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002373/abstract?rss=yes"><title>Both morning and evening dosing of nebivolol reduces trough mean blood pressure surge in hypertensive patients</title><link>http://www.ashjournal.com/article/PIIS1933171111002373/abstract?rss=yes</link><description>Abstract: The morning blood pressure surge (MBPS) has been shown to be an independent predictor of cardiovascular events. There is insufficient evidence on the effect of nebivolol, a vasodilating β1-receptor blocker, on the MBPS when given in the morning or the evening. This is a prospective, randomized, double-blind, crossover study designed to test morning vs. evening dosing of nebivolol in nondiabetic, hypertensive patients. Patients received nebivolol 5 mg/day (force-titrated to 10 mg/day after 1 week) in the morning or evening and corresponding placebos. Patients underwent ambulatory BP monitoring at baseline and after each treatment phase. Forty-two patients were randomized, of whom 38 completed both study periods. Both morning and evening dosed nebivolol significantly lowered daytime, nighttime, and 24-hour BP after 3 weeks of treatment. Evening (but not morning) dosing significantly reduced prewaking systolic BP from baseline (8.64 ± 26.46 mm Hg, P = .048). Nebivolol given in the morning or the evening significantly reduces 24-hour BP parameters. Evening dosed nebivolol may confer some advantage over morning dosing in reducing prewaking systolic BP.</description><dc:title>Both morning and evening dosing of nebivolol reduces trough mean blood pressure surge in hypertensive patients</dc:title><dc:creator>Maria Czarina Acelajado, Roberto Pisoni, Tanja Dudenbostel, Suzanne Oparil, David A. Calhoun, Stephen P. Glasser</dc:creator><dc:identifier>10.1016/j.jash.2011.09.001</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>66</prism:startingPage><prism:endingPage>72</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002403/abstract?rss=yes"><title>Differential effects of strict blood pressure lowering by losartan/hydrochlorothiazide combination therapy and high-dose amlodipine monotherapy on microalbuminuria: the ALPHABET study</title><link>http://www.ashjournal.com/article/PIIS1933171111002403/abstract?rss=yes</link><description>Abstract: We investigated the effects of losartan/hydrochlorothiazide (HCTZ) fixed combination therapy and high-dose amlodipine monotherapy on BP measurements and target organ protection. In this open-label multicenter trial, hypertensive patients were randomly allocated to receive losartan 50 mg or amlodipine 5 mg for 4 weeks, and the treatments were changed to combination of losartan 50 mg/HCTZ 12.5 mg or amlodipine 10 mg for a further 4 weeks. A total of 91 hypertensive patients (age 63.6 years), 47 in the losartan/HCTZ group and 44 in amlodipine group, were enrolled. After 8 weeks, the clinic BP, home BP, and 24-hour ambulatory BP were successfully controlled to the same level in both treatment groups (P &lt; .001). Furthermore, both groups showed the same degree of BP reduction in the 24-hour, daytime, and nighttime (P &lt; .001). B-type natriuretic peptide (BNP) also significantly decreased to the same level in both groups, whereas the reduction of urinary albumin/creatinine ratio (UACR) was greater in the losartan/HCTZ group than in the high-dose amlodipine group (–47.6% vs 2.4%, P &lt; .001). Losartan/HCTZ combination and high-dose amlodipine have similar effects on clinic, home, and ambulatory BP control and BNP reduction, whereas losartan/HCTZ has superior effect on UACR reduction when compared with high-dose amlodipine.</description><dc:title>Differential effects of strict blood pressure lowering by losartan/hydrochlorothiazide combination therapy and high-dose amlodipine monotherapy on microalbuminuria: the ALPHABET study</dc:title><dc:creator>Motoki Fukutomi, Satoshi Hoshide, Kazuo Eguchi, Tomonori Watanabe, Kazuyuki Shimada, Kazuomi Kario</dc:creator><dc:identifier>10.1016/j.jash.2011.09.004</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2011-11-04</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2011-11-04</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>73</prism:startingPage><prism:endingPage>82</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002907/abstract?rss=yes"><title>Editorial Board</title><link>http://www.ashjournal.com/article/PIIS1933171111002907/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-1711(11)00290-7</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171111002919/abstract?rss=yes"><title>Table of Contents</title><link>http://www.ashjournal.com/article/PIIS1933171111002919/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-1711(11)00291-9</dc:identifier><dc:source>Journal of the American Society of Hypertension 6, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>6</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1933-1711(11)X0008-6</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A3</prism:endingPage></item></rdf:RDF>
