Figure 1.

The proposed interaction between vitamin D and RAS metabolism. Renin catalyzes the conversion of angiotensinogen to angiotensin I, which is further converted to the vasoactive peptide angiotensin II. Angiotensin II is a direct vasoconstricter, and can also ilicit aldosterone secretion from the adrenal cortex. Under physiologic situations, activation of the RAS in response to renal-vascular hypo-perfusion serves to increase blood pressure and renal salt retention. However, in pathologic states (such as in diabetes and obesity), inappropriately high RAS activity contributes to vascular and kidney diseases. Vitamin D3 is largely produced in the skin with exposure to ultraviolet radiation, but may also be ingested orally. This precursor is hydroxylated to 25-hydroxyvitamin D (25[OH]D) and 25(OH)D serves as the stable barometer of clinical “vitamin D status.” Under the control of parathyroid hormone and calcium status, 25(OH)D can be hydroxylated to form the active vitamin D receptor (VDR) agonist 1,25-dihydroxyvitamin D (1,25[OH]2D). Activation of the VDR by 1,25(OH)2D is known to influence the regulation and expression of a myriad of genes, including renin.

Brown et al. BMC Endocrine Disorders 2013 13:33   doi:10.1186/1472-6823-13-33
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