1,25(OH)2 vitamin D3-induced alterations in vascular reactivity in the spontaneously hypertensive rat

Recent studies showed that 1,25(OH)2 vitamin D3 stimulates calcium uptake in vascular smooth muscle cells resulting in increased vascular reactivity. Despite reliable effects on vascular tissue, daily injections of 1,25(OH)2 vitamin D3 have not consistently altered basal blood pressure. In the current study, 1,25(OH)2 vitamin D3 was examined for vascular reactivity in vitro as well as blood pressure reactivity in vivo. 1,25(OH)2 vitamin D3 was either injected as a daily subcutaneous dose of 48 ng/kg or placed in an osmotic minipump that was implanted subcutaneously and delivered at a rate of 2/ng/kg/hr (48 ng/kg/d). Blood pressure reactivity to bolus injections of norepinephrine (NE) and angiotensin II (AII) was tested after 1, 6, and 7 days of 1,25(OH)2 vitamin D3 treatment. On the seventh day, the animals were killed and rings from the aorta and mesenteric artery were placed in a muscle bath for measurement of vascular reactivity to NE and potassium chloride. Vessels from animals injected with 1,25(OH)2 vitamin D3 had significantly greater responses to NE (p < 0.001) and potassium chloride (p < 0.001) than those from minipump or control animals. There was no significant difference in baseline BP across treatment conditions or any reliable difference in blood pressure reactivity to NE or AII. The data showed that 1,25(OH)2 vitamin D3 can enhance vascular reactivity without altering baseline blood pressure or blood pressure reactivity. Moreover, intermittent administration of calcitriol may enhance vascular reactivity to norepinephrine and potassium chloride to a greater extent than the same dose of calcitriol given as a continuous infusion.