1,25-Dihydroxyvitamin D3 and rat vascular smooth muscle cell growth.

Abstract

Recent studies from several laboratories have shown perturbations of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] metabolism in hypertension. While these perturbations may exert their effect on blood pressure via their actions on calcium metabolism, it is possible that this vitamin D metabolite may have direct effects on vascular smooth muscle cell (VSMC) physiology. To examine this, we studied the effect of 1,25(OH)2D3 on VSMC growth and found that this substance suppressed VSMC [3H]thymidine uptake; furthermore, this vitamin D metabolite also suppressed the stimulatory effect of epidermal growth factor (EGF) on VSMC proliferation. The concomitant presence of this substance appeared to be required for its action on VSMC growth since cells pretreated with the vitamin D metabolite for up to 72 hours and then washed of the substance grew normally and responded to EGF. Studies were also done to determine if 1,25(OH)2D3 had any effect on the function of EGF receptors on VSMC. Experiments using Iodine-125-labeled EGF showed no differences in the binding of this ligand to VSMC, either untreated or treated with 1,25(OH)2D3, which indicates the effect of the vitamin D metabolite on VSMC growth (when exposed to EGF) was not mediated by an alteration of EGF receptor function. The results of these studies have implications for the pathogenesis of vascular diseases such as hypertension and atherosclerosis.

Association between serum vitamin D levels and subclinical coronary atherosclerosis and plaque burden/composition in young adult population

“…Th ere are some mechanisms proposed to explain the relation between 25(OH)D defi ciency and coronary atherosclerosis. 25(OH)D receptor has been found in most tissues and cells, which includes vascular smooth muscle cells [15], macrophages [16], cardiomyocytes [17], endothelium [18], and lymphocytes [19]. 25(OH)D stimulates the production of prostacyclin by vascular smooth muscle cells, which prevents thrombus formation, cell adhesion, and smooth muscle cell proliferation [20].…”

Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

“…These particular changes were shown to attenuate ischemic brain disease in rodents (Wang, Wu et al 2001). In in vitro and animal models of cerebral ischemia, vitamin D inhibits antigen presenting cell maturation (Carthy, Yamashita et al 1989), down regulates NF-κB activity (Kong, Zhu et al 1999), and stimulates anti-inflammatory cytokine production (Timms, Mannan et al 2002). Epidemiological studies show an inverse association between vitamin D and C-reactive protein levels, a marker of inflammation (Timms, Mannan et al 2002).…”

Vitamin D Intake and Risk of Incident Hypertension

“…Data from animal studies implicate circulating active vitamin D as an inhibitor of renin expression in the juxtaglomerular apparatus as well as an inhibitor of vascular smooth muscle cell proliferation. 3,4 Oral supplementation with vitamin D lowers blood pressure in hypertensive rats. [5][6][7] In humans, cross-sectional data suggest an association between low vitamin D intake (Ͻ400 IU per day) and higher blood pressure, 8 and a single interventional study in vitamin D-deficient elderly women found that a combination of calcium and vitamin D supplementation had a greater blood pressure-lowering effect than calcium supplementation alone.…”