Hypertension
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Multicenter Study Comparative Study
Prevalence and risk factors for hypertension in hemophilia.
Hypertension (HTN) is a major risk factor for intracranial hemorrhage. We, therefore, investigated the prevalence, treatment, and control of HTN in adult patients with hemophilia (PWH). PWH≥18 years (n=458) from 3 geographically different cohorts in the United States were evaluated retrospectively for HTN and risk factors. ⋯ Age, body mass index, diabetes mellitus, and renal function were independently associated with HTN. Among patients with moderate or severe hemophilia there was a trend (≈1.5-fold) for higher odds of having HTN compared with patients with mild hemophilia. On the basis of these results, new care models for adult PWH and further studies for the causes of HTN in hemophilia are recommended.
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Multicenter Study Comparative Study
Social epidemiology of hypertension in middle-income countries: determinants of prevalence, diagnosis, treatment, and control in the WHO SAGE study.
Large-scale hypertension screening campaigns have been recommended for middle-income countries. We sought to identify sociodemographic predictors of hypertension prevalence, diagnosis, treatment, and control among middle-income countries. We analyzed data from 47 443 adults in all 6 middle-income countries (China, Ghana, India, Mexico, Russia, and South Africa) sampled in nationally representative household assessments from 2007 to 2010 as part of the World Health Organization Study on Global Aging and Adult Health. ⋯ Insurance status and income also emerged as significant correlates to diagnosis and treatment probability, respectively. More than 90% of hypertension cases were uncontrolled, with men having 3 times the odds as women of being uncontrolled. Overall, the social epidemiology of hypertension in middle-income countries seems to be correlated to increasing obesity prevalence, and hypertension control rates are particularly low for adult men across distinct cultures.
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Comparative Study
Functional role of TRPV4-KCa2.3 signaling in vascular endothelial cells in normal and streptozotocin-induced diabetic rats.
The small conductance and intermediate conductance Ca(2+)-activated K(+) channels are known to be involved in the endothelium-dependent hyperpolarization. Ca(2+) entry into endothelial cells stimulates these channels, causing membrane hyperpolarization in endothelial cells and underlying smooth muscle cells. In the present study, with the use of coimmunoprecipitation and double immunolabeling methods, we demonstrated a physical interaction of transient receptor potential vanilloid 4 (TRPV4) with K(Ca)2.3 in rat mesenteric artery endothelial cells. ⋯ Stimulating TRPV4-K(Ca)2.3 signaling pathway also increased local blood flow in mesenteric beds and reduced systemic blood pressure in anesthetized rats. In streptozotocin-induced diabetic rats, the expression levels of TRPV4 and K(Ca)2.3 were reduced, which could be an underlying reason for the dysfunction of endothelium-dependent hyperpolarization in these animals. These results demonstrated an important physiological and pathological role of TRPV4-K(Ca)2.3 signaling pathway in vascular endothelial cells.
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Transgenic mice with endothelium-specific endothelin-1 (ET-1) overexpression exhibit endothelial dysfunction and vascular remodeling, oxidative stress, and inflammation. We previously observed that monocytes/macrophages play a role in angiotensin II, aldosterone, and deoxycorticosterone acetate/salt-induced vascular remodeling, oxidative stress, and inflammation using a model with reduced monocytes/macrophages, the osteopetrotic (Op) mouse, which has a mutation in the macrophage colony stimulating factor (Csf1) gene. However, it is unknown whether monocytes/macrophages are implicated in adverse vascular effects of ET-1. ⋯ ET-1-induced oxidative stress measured by dihydroethidium staining (P<0.05) and NADPH oxidase activity assessed with lucigenin chemiluminescence (P<0.05) were blunted by CSF1 deficiency. ET-1 caused a 2.5-fold increase in monocyte/macrophage infiltration compared with wild-type mice (P<0.001), which was blunted in the mice deficient in CSF1. Reduction of monocyte/macrophage-dependent inflammation in mice overexpressing ET-1 in endothelium results in reduced vascular remodeling and oxidative stress, providing evidence for a role of monocytes/macrophages and innate immunity in ET-1-induced vascular injury.