Vaping, or electronic cigarette (ecig) use, is prevalent among pregnant women, although little is known about the effects of perinatal ecig use on cardiovascular health of the progeny (even when using nicotine-free e-liquid). Maternal toxicant inhalation may adversely affect vital conduit vessel development. We tested the hypothesis that perinatal exposure to maternal vaping would lead to a dose-dependent dysfunction that would persist into later life of offspring. Pregnant Sprague-Dawley rats were exposed to either nicotine-free (Ecig0) or nicotine-containing Ecig aerosol (18 mg/ml, Ecig18) starting on gestational day 2 and continued until pups were weaned (postnatal day 21). Pups were never directly exposed. Conduit artery function (stiffness and reactivity) and structure was assessed in 3- and 7-month old offspring. At 3-months, pulse wave velocity (PWV) in the ecig0 and ecig18 offspring were significantly higher than controls in both the 20-puff/day (6.6±2.1 and 4.8±1.3 vs. 3.2±0.7 m/s, respectively, p<0.05, mean ± SD) and as 60-puff/day exposure cohort (7.5 ± 2.8 and 7.5 ± 2.5 vs 3.2 ± 0.5 m/s, respectively, p<0.01). Wire myography revealed (range of 23-31%) impaired aortic relaxation in all ecig exposure groups (with or without nicotine). Incubation of vessels with TEMPOL or Febuxostat reversed the aortic dysfunction, implicating involvement of reactive oxygen species. Nearly identical changes and pattern was seen in vascular outcomes of 7-month old offspring. The take home message from this pre-clinical study is that maternal vaping during pregnancy, with or without nicotine, leads to maladaptations in vascular (aortic) development that persist into adult life of offspring.