Non-technical summary Adverse environments during early life are linked with an increased risk of cardiovascular disease. There is an alarming increase in the prevalence of vitamin D (VitD) deficiency in women of reproductive age. We show that male and female rat offspring that were exposed to VitD deficiency in the womb and early life have high blood pressure. The arteries from VitD deficient offspring have an impaired ability to relax due to deficiencies in the production of two important factors, nitric oxide and endothelium-derived hyperpolarizing factor. VitD deficient female offspring have an additional impairment in the nitric oxide signalling pathway in the arterial muscle. The findings of this study are particularly relevant for women intending to become pregnant. Ensuring VitD sufficiency before and during pregnancy in women will reduce the burden of cardiovascular disease risk in their offspring.Abstract Increasing evidence links vitamin D deficiency and cardiovascular dysfunction in human adults. There is a worldwide increase in the prevalence of vitamin D deficiency in women of reproductive age, particularly dark-skinned and/or veiled women and their infants. We used a rat model to determine the functional impact of vitamin D deficiency during intra uterine and early life on resistance artery reactivity and blood pressure in the offspring as young adults. Rat dams were maintained on vitamin D deficient or replete chow before and during pregnancy and lactation. The offspring were maintained on the same chow until studied at 7-8 weeks of age. Conscious blood pressure was measured. Endothelial and smooth muscle function were tested in mesenteric arteries on a pressure myograph. Vitamin D deficient male and female offspring had a 10-fold lower serum 25-hydroxyvitamin D (P < 0.0001) and markedly elevated blood pressures (11-20 mmHg, P < 0.001) and heart rates (21-40 beats min −1 , P < 0.02) than control fed offspring. Serum calcium was unchanged. Mesenteric artery myogenic tone was doubled in vitamin D deficiency. Endothelium-derived nitric oxide-evoked dilation was halved in arteries from vitamin D deficient males and dioestrous females. Dilation attributed to endothelium-derived hyperpolarizing factor was all but abolished in vitamin D deficient oestrous females. Nitroprusside-evoked dilation was unaltered in arteries from males, but was markedly reduced in vessels of vitamin D deplete females. In conclusion, early life vitamin D deficiency is associated with endothelial vasodilator dysfunction, and this is likely to contribute to the accompanying elevation in blood pressure and an increased cardiovascular disease risk.

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