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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D is an important prohormone for optimal intestinal calcium absorption for mineralization of bone. Because the vitamin D receptor is present in multiple tissues, there has been interest in evaluating other potential functions of vitamin D, particularly, in cardiovascular diseases (CVD). Cross-sectional studies have reported that vitamin D deficiency is associated with increased risk of CVD, including hypertension, heart failure, and ischemic heart disease. Initial prospective studies have also demonstrated that vitamin D deficiency increases the risk of developing incident hypertension or sudden cardiac death in individuals with preexisting CVD. Very few prospective clinical studies have been conducted to examine the effect of vitamin D supplementation on cardiovascular outcomes. The mechanism for how vitamin D may improve CVD outcomes remains obscure; however, potential hypotheses include the downregulation of the renin-angiotensin-aldosterone system, direct effects on the heart, and vasculature or improvement of glycemic control. This review will examine the epidemiologic and clinical evidence for vitamin D deficiency as a cardiovascular risk factor and explore potential mechanisms for the cardioprotective effect of vitamin D.
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PMID:Vitamin D deficiency and risk for cardiovascular disease. 1959 2

Cardiovascular disease (CVD) is a major cause of morbidity and mortality worldwide. Recently vitamin D deficiency has been identified as a potential risk factor for many diseases not traditionally associated with vitamin D, such as cancer and CVD. This review discusses the evidence suggesting an association between low 25-hydroxyvitamin D levels and CVD and the possible mechanisms mediating it. Vitamin D deficiency has been associated with CVD risk factors such as hypertension and diabetes mellitus, with markers of subclinical atherosclerosis such as intima-media thickness and coronary calcification as well as with cardiovascular events such as myocardial infarction and stroke as well as congestive heart failure. It could be suggested that vitamin D deficiency contributes to the development of CVD through its association with risk factors, such as diabetes and hypertension. However, direct effects of vitamin D on the cardiovascular system may also be involved. Vitamin D receptors are expressed in a variety of tissues, including cardiomyocytes, vascular smooth muscle cells and endothelial cells and vitamin D has been shown to affect inflammation and cell proliferation and differentiation. While much evidence supports a potential antiatherosclerotic effect of vitamin D, prospective, placebo-controlled randomized as well as mechanistic studies are needed to confirm this association. Since vitamin D deficiency is easy to screen for and treat, the confirmation of such an association could have important implications for both, patient care and health policy.
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PMID:Vitamin D and cardiovascular disease. 1960 65

Vitamin D insufficiency/deficiency has been worldwide reported in all age groups in recent years. It has been considered a Public Health matter since decreased levels of vitamin D has been related to several chronic diseases, as type 2 diabetes mellitus (T2DM), obesity and hypertension. Glucose intolerance and insulin secretion has been observed during vitamin D deficiency, both in animals and humans resulting in T2DM. The supposed mechanism underlying these findings is presence of vitamin D receptor in several tissues and cells, including pancreatic beta-cells, adipocyte and muscle cells. In obese individuals, the impaired vitamin D endocrine system, characterized by high levels of PTH and 1,25(OH)(2)D(3) could induce a negative feedback for the hepatic synthesis of 25(OH)D and also contribute to a higher intracellular calcium, which in turn secrete less insulin and deteriorate insulin sensitivity. In hypertension, vitamin D could act on renin-angiotensin system and also in vascular function. Administration of 1,25(OH)(2)D(3) could decreases renin gene expression and inhibit vascular smooth muscle cell proliferation. However, prospective and intervention human studies that clearly demonstrates the benefits of vitamin D status adequacy in the prevention and treatment of endocrine metabolic diseases are lacking. Further research still necessary to assure the maximum benefit of vitamin D in such situations.
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PMID:[Vitamin D and endocrine diseases]. 1976 53

Vitamin D receptors have been detected in vascular smooth muscle cells, and 1,25-dihydroxyvitamin D inhibits the renin mRNA expression. Epidemiological studies show an inverse relation between serum 25-hydoxyvitamin D levels and blood pressure, and low serum 25-hydoxyvitamin D levels are reported to be predictors of future development of hypertension. This may indicate an important role for vitamin D in blood pressure regulation. In the present study, 25-hydoxyvitamin D was measured in sera collected in 1994 from 4125 subjects who did not use blood pressure medication, and thereafter measurement was repeated in 2008 for 2385 of these subjects. In sera from 1994 there was a significant decrease in age, body mass index, and systolic blood pressure and a significant increase in physical activity score across increasing 25-hydoxyvitamin D quartiles. After adjusting for sex, age, body mass index, and physical activity, the difference in systolic blood pressure between the lowest and highest serum 25-hydoxyvitamin D quartiles was 3.6 mm Hg. After adjustment for confounders, serum 25-hydoxyvitamin D from 1994 did not predict future hypertension or increase in blood pressure, nor was there any significant association between change in serum 25-hydoxyvitamin D from 1994 to 2008 and change in blood pressure. Our results do not support a causal role for vitamin D in blood pressure regulation, and large randomized clinical trials, preferably including subjects with hypertension and/or low serum 25-hydoxyvitamin D levels, are greatly needed to clarify whether vitamin D supplementation affects the blood pressure.
Hypertension 2010 Mar
PMID:Serum 25-hydroxyvitamin D levels are strongly related to systolic blood pressure but do not predict future hypertension. 2006 52

Vitamin D regulates the renin-angiotensin system (RAS) in experimental animals, but corresponding human data are limited. We examined the relation between plasma 25-hydroxyvitamin D and elements of the RAS in 184 normotensive individuals in high sodium balance; these included circulating levels of plasma renin activity and angiotensin II (Ang II) and the renal plasma flow response to infused Ang II, which is an indirect measure of the intrinsic RAS activity in the kidney. Compared with individuals with sufficient 25-hydroxyvitamin D levels (> or = 30.0 ng/mL), those with insufficiency (15.0 to 29.9 ng/mL) and deficiency (<15.0 ng/mL) had higher circulating Ang II levels (P for trend=0.03). Moreover, those with vitamin D deficiency had significantly blunted renal plasma flow responses to infused Ang II (mean decrease of 115 mL/min per 1.73 m(2) in renal plasma flow versus 145 mL/min per 1.73 m(2) among those with sufficient vitamin D levels; P for trend=0.009). Although plasma renin activity was higher among individuals with insufficient levels of vitamin D, the result was not statistically significant. These data suggest that low plasma 25-hydroxyvitamin D levels may result in upregulation of the RAS in otherwise healthy humans.
Hypertension 2010 May
PMID:Plasma 25-hydroxyvitamin D and regulation of the renin-angiotensin system in humans. 2035 44

Vitamin D has been reported to lower blood pressure in vivo by regulating the renin-angiotensin system; however, there are limited clinical studies to support this finding in humans. We investigated the effect of vitamin D treatment on hypertension in a three-arm randomized placebo controlled pilot and feasibility study. We tested placebo with two forms of vitamin D: cholecalciferol (vitamin D(3)) and the active form of vitamin D, calcitriol. Subjects were recruited from the Atlanta Veterans Affairs Medical Center in Decatur, GA between April and August 2008. Subjects received 200,000IU of vitamin D(3) (n=3) weekly for 3 weeks or matching placebo (n=3) weekly for 3 weeks (n=3) or 0.5mug calcitriol (n=2) taken twice daily for one week. Our primary endpoint was blood pressure measured by 24h ambulatory blood pressure monitor. Subjects receiving calcitriol experienced a 9% decrease in mean systolic blood pressure (SBP) compared placebo (p<0.001). One week after conclusion of calcitriol therapy SBP returned to pre-treatment levels. There was no reduction in blood pressure in the placebo or vitamin D(3) groups. Results from this pilot study suggests that active vitamin D therapy may be an effective short-term intervention for reducing blood pressure and needs to be explored further in larger controlled studies.
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PMID:1,25-dihydroxyvitamin D3 reduces systolic blood pressure in hypertensive adults: a pilot feasibility study. 2042 Sep 7

The epidemiological profile of the HIV virus has undergone substantial modifications with advances in antiretroviral therapy. There has been a sharp decline in morbi-mortality levels of HIV-infected patients, which has resulted in higher survival rates. The HIV seropositive population is living longer and more exposed to chronic complications caused by the disease itself and the prolonged use of antiretrovirals. Initially, metabolic alterations were reported, increasing cardiovascular disease risk. Subsequently, damage on bone metabolism was related. Vitamin D insufficiency has now reached epidemic proportions, even in healthy individuals living in the tropics. Recent data suggest the hypovitaminosis D association with metabolic syndrome, immune diseases, diabetes and hypertension. Little is known regarding the effects of HIV/Aids and its treatment on the metabolism of vitamin D. In HIV-positive patients, factors linked to the virus itself and the use of antiretrovirals may be added to the other causes of hypovitaminosis D.
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PMID:Vitamin D deficiency in HIV-infected individuals: one more risk factor for bone loss and cardiovascular disease? 2048 99

Vitamin D has been known to medical science for almost a century. Yet, it is only in the last 15 years that we have realized that the biological effects of vitamin D extend far beyond the control of calcium metabolism. Recent observational evidence suggests strong links between low vitamin D levels and a range of cardiovascular conditions, including stroke, myocardial infarction, hypertension, and diabetes. Interventional studies are beginning to explore whether vitamin D supplementation can modify vascular health and prevent cardiovascular disease. This article reviews the physiology and function of vitamin D, examines the current observational and intervention data in cardiovascular disease, and discusses future research and current practice recommendations.
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PMID:Vitamin D and cardiovascular prevention. 2055 79

The increasing worldwide displacement from the natural outdoor environment of human beings to an indoor sedentary lifestyle, along with the recommendation to avoid any direct sun exposure because of the risk of skin cancer, has resulted in a global pandemic of vitamin D insufficiency. Traditionally, vitamin D has been associated primarily with bone health. However, it has become evident that adequate vitamin D status is important for optimal function of many organs and tissues throughout the body, including the cardiovascular system. Vitamin D insufficiency seems to predispose to hypertension, diabetes and the metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. The relationship between baseline vitamin D status, dose of vitamin D supplements, and cardiovascular events remains to be investigated by ongoing randomized trials; however increasing evidence suggests that the provision of a simple, well-tolerated, and inexpensive correction of vitamin D insufficiency favourably affects the morbility and mortality of cardiovascular disease along with the prevention of the most common chronic degenerative diseases.
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PMID:[Vitamin D deficiency and cardiovascular diseases]. 2059 17

Chronic kidney disease (CKD) independently increases the rates of cardiovascular disease, whereas the severity of kidney disease correlates with increased cardiovascular morbidity and death. Vitamin D is modified in the liver and the kidney to its active form (1,25-dihydroxyvitamin D) by the 25-hydroxy vitamin D 1-hydroxylase enzyme (CYP27B1). The activated vitamin D brings about its actions through the vitamin D receptor (VDR). The VDRs and CYP27B1 have recently been shown to be expressed in several tissues, not directly involved in mineral homeostasis, including the cardiovascular, immune, and epithelial systems. The action of vitamin D in these tissues is implicated in the regulation of endothelial, vascular smooth muscle, and cardiac cell function, the renin-angiotensin system, inflammatory and fibrotic pathways, and immune response. Impaired VDR activation and signalling results in cellular dysfunction in several organs and biological systems, which leads to reduced bone health, an increased risk for epithelial cancers, metabolic disease, and uncontrolled inflammatory responses. Failure of cardiovascular VDR activation results in hypertension, accelerated atherosclerosis and vascular calcification, cardiac hypertrophy with vascular rarification and fibrosis, and progressive renal dysfunction. An emerging body of evidence has prompted attention to the relationship between CKD, mineral bone disorder (CKD-MBD), and cardiovascular disease in the new guidelines from Kidney Disease: Improving Global Outcomes. Vitamin D receptor activators, commonly used to treat CKD-MBD, and an appropriate treatment of vitamin D hormonal system failure in patients with CKD, may help to reduce cardiovascular morbidity and mortality in these patients.
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PMID:The vitamin D system: a crosstalk between the heart and kidney. 2060 45


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