1,25-dihydroxyvitamin D3 binds specifically to rat vascular smooth muscle cells and stimulates their proliferation in vitro

Koh, Eio; Morimoto, Shigeto; Fukuo, Keisuke; Itoh, Kazuyuki; Hatori, Takashi; Shiraishi, Tsunehito; Onishi, Toshio; Kumahara, Yuichi

doi:10.1016/0024-3205(88)90685-6

Cited by 47 publications

(22 citation statements)

References 21 publications

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“…104 This is probably caused by the stimulation of migration 12 and proliferation of smooth muscle cells. 79,105,106 Recently, the combination of vitamin D 2 and cholesterol has been used to induce both peripheral atherosclerosis and aortic valve stenosis in a rabbit model. 107 In this model, the addition of vitamin D 2 to the high cholesterol diet resulted in significantly higher levels of circulating cholesterol.…”

Section: Norman and Powellmentioning

confidence: 99%

Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries

Norman

Powell

2005

ATVB

104

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Abstract-Vitamin D is generally associated with calcium metabolism, especially in the context of uptake in the intestine and the formation and maintenance of bone. However, vitamin D influences a wide range of metabolic systems through both genomic and nongenomic pathways that have an impact on the properties of peripheral arteries. The genomic effects have wide importance for angiogenesis, elastogenesis, and immunomodulation; the nongenomic effects have mainly been observed in the presence of hypertension. Although some vitamin D is essential for cardiovascular health, excess may have detrimental effects, particularly on elastogenesis and inflammation of the arterial wall. Vitamin D is likely to have a role in the paradoxical association between arterial calcification and osteoporosis. This review explores the relationship between vitamin D and a range of physiological and pathological processes relevant to peripheral arteries. ( T he primary role of vitamin D and its active metabolites is maintaining calcium homeostasis by increasing intestinal calcium absorption and, depending on circulating calcium levels, influencing the balance between bone resorption and formation. The physiological role of vitamin D in skeletal and cellular health has been reviewed elsewhere. 1 Vitamin D also has effects on the microendocrine systems of the vasculature, some of which have only been appreciated recently. This review reflects on the possible influence of vitamin D on peripheral arterial disease, which includes diseases (both occlusive and dilating) of the abdominal aorta and the distal arteries supplying the lower limb. Atherosclerosis is a major contributor to peripheral arterial disease, but the risk factors are subtly different from those for coronary artery disease: smoking is the dominating risk factor for peripheral arterial disease. Does vitamin D have any influence on the disease process? Vitamin D Metabolites and AnaloguesCholecalciferol is a prohormone that is synthesized in the skin by photochemical conversion of 7-dehydrocholesterol ( Figure 1). It is subsequently hydroxylated to Nongenomic EffectsIn common with other steroid hormones, 1␣,25(OH) 2 D 3 induces a range of effects which occur too rapidly to involve gene expression. These include increases in intracellular calcium and cGMP levels, activation of protein kinase C and changes in phosphinositide metabolism 11 (Figure 2). The effects are known to be mediated by 1 or more plasma membrane receptors, but their role is unclear in most cell types. 2,11 An example relevant to the arterial wall includes the stimulation of vascular smooth muscle cell (VSMC) migration through activation of phosphatidylinositol 3-kinase. 12 Target Cells and Tissues for 1␣,25(OH) 2 D 3Classically, the action of 1␣,25(OH) 2 D 3 is to maintain calcium and phosphate homeostasis, with the intestine and bone being key targets. It also acts on a wide range of nonclassical target tissues, including the heart and arterial wall. 13 The influence of 1␣,25(OH) 2 D 3 on these tissues could...

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Section: Norman and Powellmentioning

confidence: 99%

Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries

Norman

Powell

2005

ATVB

104

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“…Specific receptors for 1,25(OH)2D have been found on cardiac muscle (31), vascular smooth muscle (32) and endothelial cells (33). It has been shown that 1,25(OH)2D stimulates calcium uptake (34), calcium-ATPase activity (35) and proliferation of vascular smooth muscle cells (36). When administered to humans, 1,25(OH)2D caused elevation of the blood pressure (37), and augmented the pressor response to norepinephrine in spontaneously hypertensive rats (SHR) (38).…”

Section: Fig 4 Correlation Between Serum Intact Parathyroid Hormonementioning

confidence: 99%

High Blood Pressure, Bone-Mineral Loss and Insulin Resistance in Women

et al. 2005

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“…The serum concentration of this active metabolite of vitamin D has been reported by some to be unchanged [18, 23]and by others to be elevated [16, 22]in hypertensive as compared with normotensive individuals. The receptor of calcitriol has been shown in vascular smooth muscle cells [64, 65], and calcitriol also stimulates the capture of calcium from the extracellular space [66, 67, 68, 69, 70]. Moreover, treatment with calcitriol increases the force-generating capacity of isolated resistance arteries [66, 69]and enhances the pressor response to norepinephrine and angiotensin II in vivo [71].…”

Section: Introductionmentioning

confidence: 99%

Parathyroid Hormone and Calcitriol in Hypertension Caused by Dietary Calcium Deficiency in Rats

López‐Miranda

Civantos²,

Blasco³

et al. 1998

J Vasc Res

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Hypertension caused by calcium deficiency in the diet has been linked with an increase in parathyroid hormone (PTH) and calcitriol levels. We evaluated arterial blood pressure (ABP), PTH, and calcitriol in normotensive Sprague-Dawley rats (SDR) and in spontaneously hypertensive rats (SHR) fed from weaning on a control diet with a normal calcium content (1%) or a low-calcium diet (0.1%). The calcemia was also measured in the rats by colorimetric methods. The low-calcium diet decreased the calcemia in both strains and brought about an increase in the ABP which was significant in adult SDR and particularly noticeable during the early hypertensive phase in SHR. The rats fed on this diet had higher hormonal plasma levels when compared with the corresponding values in rats fed on the control diet. In particular, the SDR fed on the low-calcium diet showed much higher PTH (122.6 ± 31.0 pg/ml, p ≤ 0.05) and calcitriol (458.0 ± 13.1 pg/ml, p ≤ 0.01) values than the SDR fed on the control diet (PTH 31.7 ± 2.80 pg/ml; calcitriol 292.1 ± 17.5 pg/ml). These endocrine alterations could justify the increase in ABP caused by dietary calcium deficiency in normotensive rats. Nevertheless, the results of this study indicate that the modifications of the ABP caused by the low-calcium diet in SHR could not be correlated with significant increases in these hormones.

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1,25-dihydroxyvitamin D3 binds specifically to rat vascular smooth muscle cells and stimulates their proliferation in vitro

Cited by 47 publications

References 21 publications

Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries

Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries

High Blood Pressure, Bone-Mineral Loss and Insulin Resistance in Women

Parathyroid Hormone and Calcitriol in Hypertension Caused by Dietary Calcium Deficiency in Rats

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