维生素D、维生素D受体与高血压

人体维生素D主要来自阳光照射皮肤后合成和饮食摄入，其经典作用是通过维生素D受体（VDR）介导调节骨钙代谢，此外，脑、胰腺、心脏、血管以及免疫细胞等也存在VDR，配体激活的VDR可调节许多基因表达。研究表明维生素D负性调节肾素一血管紧张素系统，对心血管具有潜在的作用，流行病学资料提示维生素D缺乏与高血压关联。维生素D不足发生率高，进一步明确维生素D不足在高血压中的作用并采取相应措施对高血压的防治具有重要意义。     

维生素D、维生素D受体与高血压

人体维生素D主要来自阳光照射皮肤后合成和饮食摄入,其经典作用是通过维生素D受体(VDR)介导调节骨钙代谢,此外,脑、胰腺、心脏、血管以及免疫细胞等也存在VDR,配体激活的VDR可调节许多基因表达.研究表明维生素D负性调节肾素-血管紧张素系统,对心血管具有潜在的作用,流行病学资料提示维生素D缺乏与高血压关联.维生素D不足发生率高,进一步明确维生素D不足在高血压中的作用并采取相应措施对高血压的防治具有重要意义.     

1,25二羟维生素D3的心血管系统保护作用研究进展

1,25二羟维生素D3除调节人体内钙磷平衡外,在心血管系统还具有重要作用.临床研究发现,1,25二羟维生素D3缺乏可使罹患高血压、冠心病及心功能不全危险性增加.其保护心血管疾病的机制可能包括以下三个方面:调节肾素-血管紧张素系统;抑制心肌肥厚和心肌细胞增殖;抗炎、抗动脉粥样硬化和血管保护作用.     

脑梗死患者血管紧张素转化酶基因多态性与血浆血管紧张素Ⅱ水平研究

探讨脑梗死患者血管紧张素转化酶基因多态性与血浆血管紧张素Ⅱ水平的关系。应用聚合酶链反应测定 173例高血压脑梗死患者血管紧张素转化酶基因插入 /缺失 (D/I)多态性以及用酶联免疫吸附测定法测定血浆血管紧张素Ⅱ水平 ,并与正常对照组比较。结果发现 ,脑梗死组血管紧张素转化酶DD基因型频率为 0 .39,明显高于对照组的 0 .2 4 (P <0 .0 1)。进一步分析发现这种异常与发病年龄≤ 6 0岁组血管紧张素转化酶DD基因型频率明显增高有关。脑梗死组中血浆血管紧张素Ⅱ水平为 2 9.8± 10 .2ng/L ,与对照相比差异无显著性意义 (P >0 .0 5 ) ,但血管紧张素转化酶DD基因型者血浆血管紧张素Ⅱ水平显著高于对照组和同组DI基因型和Ⅱ基因型者 (P <0 .0 1)。发病年龄≤ 6 0岁血管紧张素转化酶DD基因型者血浆血管紧张素Ⅱ水平增高最明显。结果提示 ,血管紧张素转化酶DD基因型是脑梗死发病危险因素 ,发病年龄小于 6 0岁的脑梗死者可能与血管紧张素转化酶D等位基因频率增高、血浆血管紧张素Ⅱ水平增高有关。     

维生素D的水平与血管健康相关

最近,每日科学报道:即使对于正常人,缺乏维生素D与动脉僵化及血管无法舒张有相关联。研究进一步证实维生素D缺乏可导致血管健康受损,引发高血压及心血管疾病风险。参与研究的受试者通过提高维生素D水     

局部肾素—血管紧张素系统与高血压

近年来对高血压发病机理的研究取得了一些进展。其发病机理可能与多种因素有关,本文着重介绍局部肾素-血管紧张素系统与高血压的关系。     

维生素D对心血管疾病影响的研究进展

维生素D参与内分泌、炎症等多种功能。维生素D缺乏与高血压、高血脂症、心肌梗死、中风、慢性肾脏病及2型糖尿病等疾病的发生率升高有关。低维生素D水平会上调肾素-血管紧张素-醛固酮系统，促进炎症并引起内皮功能障碍。本文就维生素D对心血管疾病的影响的研究进展作一综述。     

维生素D与血压调节的关系

维生素D缺乏十分常见,其可能通过激活肾素-血管紧张素-醛固酮系统(RAS),引起继发性甲状旁腺功能亢进及影响内皮功能等机制影响血压。不同年龄人群的维生素D缺乏与血压存在着关系,但补充维生素D对血压的影响在不同研究中存在差异。     

维生素D与心血管疾病关系研究进展

维生素D不仅对人体钙磷代谢和骨质钙化有重要作用,而且对全身各组织细胞都有广泛作用,与各种重要疾病均有密切关系。其中,维生素D缺乏与心血管疾病关系日益受到国际医学界的重视。其可能通过增加甲状旁腺激素、激活肾素-血管紧张素-醛固酮系统、增加胰岛素抵抗等机制对心血管系统产生不良影响,引起高血压、左室肥厚、代谢综合征、系统炎症,从而增加动脉粥样硬化和心血管事件。目前,在我国大多数医院都没有维生素D的检验项目,且缺乏有关维生素D水平的流行病学资料,许多医务人员和科研人员对其认识仅还停留在对钙磷代谢的影响上。本文就维生素D缺乏与心血管疾病的关系以及补充维生素D降低心血管事件等方面临床研究作一系统回顾,以期引起我国学者对维生素D的重视,加强相关研究。     

维生素D与代谢综合征

维生素D是人体必需的营养物质,其功能主要是通过维生素D受体来介导的.近年来研究发现,维生素D对胰岛具有保护作用,并且是维持正常胰岛素分泌和糖耐昔所必需的物质.临床及动物模型研究已证实维生素D对保证胰岛素正常释放以及维持糖耐量正常是必不可少的.维生素D受体基因多态性可能影响脂肪形成以及胰岛素敏感性.维生素D缺乏不仅与胰岛素抵抗和高血压的发生直接相关,而且可显著增加代谢综合征的发病风险.     

Interplay of vitamin D and metabolic syndrome: A review

Vitamin D deficiency is a worldwide public health problem. Vitamin D deficiency plays key role in the pathophysiology of risk factors of metabolic syndrome which affect cardiovascular system, increase insulin resistance and obesity, stimulate rennin–angiotensin–aldosterone system that cause hypertension. The discovery of vitamin D receptor expressed ubiquitously in almost all body cells such as immune, vascular and myocardial cells, pancreatic beta cells, neurons and osteoblasts suggests an involvement of vitamin D mediated effects on metabolic syndrome. Moreover vitamin D deficiency as well as cardiovascular diseases and related risk factors frequently co-occur. This underlines the importance of understanding the role of vitamin D in the context of metabolic syndrome. The paper provides an insight into the physiology of vitamin D and relationship of vitamin D deficiency with risk factors of metabolic syndrome through observational and supplementation studies.     

维生素D状态与心血管危险

已知维生素D最重要的功能是维持人体钙离子代谢的平衡。近些年来的研究发现维生素D受体广泛存在于人体的多种组织细胞中,因此维生素D是否还具有其他重要的生物学功能成为研究热点,其中维生素D缺乏与心血管风险的关系颇为引人注目。一些研究提示维生素D缺乏可能增加心血管风险,包括高血压、心力衰竭和缺血性心脏病等。但其致病机制和影响程度尚不十分明确。现综述了目前有关维生素D状态与心血管危险间关系的假设机制,并探讨为验证有关假设已进行的一些重要研究。     

Vitamin D and Cardiovascular Risk

Vitamin D deficiency is a common condition that has well-documented effects on musculoskeletal health. A growing body of literature has related vitamin D deficiency to other chronic disorders, including cardiovascular disease. Several plausible biological mechanisms have been postulated to explain this association, including the effect of poor vitamin D status on intermediate risk factors (eg, hypertension and diabetes), neurohormonal activation, inflammation, and cardiac remodeling. These mechanisms have been explored in experimental and animal studies, as well as several small interventional studies. The results of the controlled trials have not been conclusive to date. In this review, we summarize the existing studies investigating the effects of vitamin D on cardiovascular health, and propose that additional well-designed, prospective, randomized controlled trials are necessary to delineate the appropriate role of vitamin D supplementation in reducing the burden of cardiovascular disease.     

Vitamin D and the elderly

This review summarizes current knowledge on vitamin D status in the elderly with special attention to definition and prevalence of vitamin D insufficiency and deficiency, relationships between vitamin D status and various diseases common in the elderly, and the effects of intervention with vitamin D or vitamin D and calcium. Individual vitamin D status is usually estimated by measuring plasma 25-hydroxyvitamin D (25OHD) levels. However, reference values from normal populations are not applicable for the definition of vitamin D insufficiency or deficiency. Instead vitamin D insufficiency is defined as the lowest threshold value for plasma 25OHD (around 50 nmol/l) that prevents secondary hyperparathyroidism, increased bone turnover, bone mineral loss, or seasonal variations in plasma PTH. Vitamin D deficiency is defined as values below 25 nmol/l. Using these definitions vitamin D deficiency is common among community-dwelling elderly in the developed countries at higher latitudes and very common among institutionalized elderly, geriatric patients and patients with hip fractures. Vitamin D deficiency is an established risk factor for osteoporosis, falls and fractures. Clinical trials have demonstrated that 800 IU (20 microg) per day of vitamin D in combination with 1200 mg calcium effectively reduces the risk of falls and fractures in institutionalized patients. Furthermore, 400 IU (10 microg) per day in combination with 1000 mg calcium or 100 000 IU orally every fourth month without calcium reduces fracture risk in individuals over 65 years of age living at home. Yearly injections of vitamin D seem to have no effect on fracture risk probably because of reduced bioavailability. Simulation studies suggest that fortification of food cannot provide sufficient vitamin D to the elderly without exceeding present conventional safety levels for children. A combination of fortification and individual supplementation is proposed. It is argued that all official programmes should be evaluated scientifically. Epidemiological studies suggest that vitamin D insufficiency is related to a number of other disorders frequently observed among the elderly, such as breast, prostate and colon cancers, type 2 diabetes, and cardiovascular disorders including hypertension. However, apart from hypertension, causality has not been established through randomized intervention studies. It seems that 800 IU (20 microg) vitamin D per day in combination with calcium reduces systolic blood pressure in elderly women.     

Vitamin D deficiency: Implications for acute care in the elderly and in patients with chronic illness

There is evidence that the vast majority of hospitalized patients have vitamin D deficiency. Vitamin D deficiency is a poorly recognized pandemic with evidence to indicate inadequate testing and monitoring of response to treatment in high‐risk populations. Vitamin D receptors are ubiquitous in the human body and while the endocrine effects of vitamin D are well recognized, the autocrine and paracrine effects of this steroid hormone are less well appreciated. These functions include antimicrobial and immunomodulation effects as well benefits on cardiovascular health, autoimmune disease, cancer and metabolism. Vitamin D deficiency increases mortality and even a modest amount of vitamin D may enhance longevity. Emerging evidence suggests that a vitamin D replete state carries significant health benefits in acute illness. In this review, we discuss the role of vitamin D deficiency and potential benefits in treating this deficiency focusing on the implications for managing acute illness in elderly patients and those with an underlying chronic illness. Geriatr Gerontol Int 2011; 11: 395–407.     

Vitamin D, cardiovascular disease and mortality

A poor vitamin D status, i.e. low serum levels of 25-hydroxyvitamin D [25(OH)D], is common in the general population. This finding is of concern not only because of the classic vitamin D effects on musculoskeletal outcomes, but also because expression of the vitamin D receptor (VDR) and vitamin D metabolizing enzymes in the heart and blood vessels suggests a role of vitamin D in the cardiovascular system. VDR-knockout mice suffer from cardiovascular disease (CVD), and various experimental studies suggest cardiovascular protection by vitamin D, including antiatherosclerotic, anti-inflammatory and direct cardio-protective actions, beneficial effects on classic cardiovascular risk factors as well as suppression of parathyroid hormone (PTH) levels. In epidemiological studies, low levels of 25(OH)D are associated with increased risk of CVD and mortality. Data from randomized controlled trials (RCTs) are sparse and have partially, but not consistently, shown some beneficial effects of vitamin D supplementation on cardiovascular risk factors (e.g. arterial hypertension). We have insufficient data on vitamin D effects on cardiovascular events, but meta-analyses of RCTs indicate that vitamin D may modestly reduce all-cause mortality. Despite accumulating data suggesting that a sufficient vitamin D status may protect against CVD, we still must wait for results of large-scale RCTs before raising general recommendations for vitamin D in the prevention and treatment of CVD. In current clinical practice, the overall risks and costs of vitamin D supplementation should be weighed against the potential adverse consequences of untreated vitamin D deficiency.     

Can vitamin D deficiency cause diabetes and cardiovascular diseases? Present evidence and future perspectives

Several studies have shown that vitamin D may play a role in many biochemical mechanisms in addition to bone and calcium metabolism. Recently, vitamin D has sparked widespread interest because of its involvement in the homeostasis of the cardiovascular system. Hypovitaminosis D has been associated with obesity, related to trapping in adipose tissue due to its lipophilic structure. In addition, vitamin D deficiency is associated with increased risk of cardiovascular disease (CVD) and this may be due to the relationship between low vitamin D levels and obesity, diabetes mellitus, dyslipidaemia, endothelial dysfunction and hypertension. However, although vitamin D has been identified as a potentially important marker of CVD, the mechanisms through which it might modulate cardiovascular risk are not fully understood. Given this background, in this work we summarise clinical retrospective and prospective observational studies linking vitamin D levels with cardio-metabolic risk factors and vascular outcome. Moreover, we review various randomised controlled trials (RCTs) investigating the effects of vitamin D supplementation on surrogate markers of cardiovascular risk. Considering the high prevalence of hypovitaminosis D among patients with high cardiovascular risk, vitamin D replacement therapy in this population may be warranted; however, further RCTs are urgently needed to establish when to begin vitamin D therapy, as well as to determine the dose and route and duration of administration.     

Protective links between vitamin D,inflammatory bowel disease and colon cancer

Vitamin D deficiency has been associated with a wide range of diseases and multiple forms of cancer including breast, colon, and prostate cancers. Relatively recent work has demonstrated vitamin D to be critical in immune function and therefore important in inflammatory diseases such as inflammatory bowel disease(IBD). Because vitamin D deficiency or insufficiency is increasingly prevalent around the world, with an estimated 30%-50% of children and adults at risk for vitamin D deficiency worldwide, it could have a significant impact on IBD. Epidemiologic studies suggest that low serum vitamin D levels are a risk factor for IBD and colon cancer, and vitamin D supplementation is associated with decreased colitis disease activity and/or alleviated symptoms. Patients diagnosed with IBD have a higher incidence of colorectal cancer than the general population, which supports the notion that inflammation plays a key role in cancer development and underscores the importance of understanding how vitamin D influences inflammation and its cancer-promoting effects. In addition to human epidemiological data, studies utilizing mouse models of colitis have shown that vitamin D is beneficial in preventing or ameliorating inflammation and clinical disease. The precise role of vitamin D on colitis is unknown; however, vitamin D regulates immune cell trafficking and differentiation, gut barrier function and antimicrobial peptide synthesis, all of which may be protective from IBD and colon cancer. Here we focus on effects of vitamin D on inflammation and inflammation-associated colon cancer and discuss the potential use of vitamin D for protection and treatment of IBD and colon cancer.     

Vitamin D and Vascular Disease: The Current and Future Status of Vitamin D Therapy in Hypertension and Kidney Disease

Over the past decade, vitamin D has generated considerable interest as potentially having important effects on the vasculature and the kidney. Animal and human data indicate that vitamin D suppresses the activity of the renin-angiotensin system and improves endothelial function. Observational studies in humans suggest that low 25-hydroxyvitamin D (25[OH]D) levels are associated with a higher risk of hypertension. However, findings from randomized trials of vitamin D supplementation (with cholecalciferol or ergocalciferol) to lower blood pressure are inconsistent, possibly stemming from variability in study population, sample size, vitamin D dose, and duration. Supplementation with activated vitamin D (i.e., 1,25-dihydroxyvitamin D or analogues) in patients with chronic kidney disease reduces urine albumin excretion, an important biomarker for future decline in renal function. These studies are reviewed, with special emphasis on recent findings. Definitive studies are warranted to elucidate the effects of vitamin D supplementation on mechanisms of hypertension and kidney disease.     

Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease

Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. Cholesterol and vitamin D share the 7-dehydrocholesterol metabolic pathway. This study evaluated the possible effect of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. After diagnosis, patients received atorvastatin as secondary prevention. Serum vitamin D was measured by high-performance liquid chromatography at baseline and at 12 months. Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels (41+/-19 vs 47+/-19 nmol/L, p=0.003). Vitamin D deficiency was decreased by 75% to 57% at 12 months. In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels.