ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Maternal nutrient restriction during pregnancy impairs an endothelium-derived hyperpolarizing factor-like pathway in sheep fetal coronary arteries.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Integrating endothelium-derived hyperpolarization, nitric oxide, and prostacyclin pathways: the multimodal potential of human tissue kallikrein-1.Vascular biology (Bristol, England) · 2025Review
- Maternal Undernutrition during Pregnancy Alters Amino Acid Metabolism and Gene Expression Associated with Energy Metabolism and Angiogenesis in Fetal Calf Muscle.Metabolites · 2021Article
- Insights into the Mechanisms of Fetal Growth Restriction-Induced Programming of Hypertension.Integrated blood pressure control · 2021Review
- Increased susceptibility to cardiovascular disease in offspring born from dams of advanced maternal age.The Journal of physiology · 2018Article
- Roles of angiotensin II type 2 receptor in mice with fetal growth restriction.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Passive Stretch Induces Structural and Functional Maturation of Engineered Heart Muscle as Predicted by Computational Modeling.Stem cells (Dayton, Ohio) · 2018Article
- Paracrine Effects of the Pluripotent Stem Cell-Derived Cardiac Myocytes Salvage the Injured Myocardium.Circulation research · 2017Article
- Partial Reprogramming of Pluripotent Stem Cell-Derived Cardiomyocytes into Neurons.Scientific reports · 2017Article
- Developmental conditioning of endothelium-derived hyperpolarizing factor-mediated vasorelaxation.Journal of hypertension · 2016Article
- Development of a scalable suspension culture for cardiac differentiation from human pluripotent stem cells.Stem cell research · 2015Article
- 5-hydroxytryptamine has an endothelium-derived hyperpolarizing factor-like effect on coronary flow in isolated rat hearts.Journal of biomedical science · 2015Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms underlying developmental programming are poorly understood but may be associated with adaptations by the fetus in response to changes in the maternal environment during pregnancy. We hypothesized that maternal nutrient restriction during pregnancy alters vasodilator responses in fetal coronary arteries. Pregnant ewes were fed a control [100% U.S. National Research Council (NRC)] or nutrient-restricted (60% NRC) diet from days 50 to 130 of gestation (term = 145 days); fetal tissues were collected at day 130. In coronary arteries isolated from control fetal lambs, relaxation to bradykinin was unaffected by nitro-l-arginine (NLA). Iberiotoxin or contraction with KCl abolished the NLA-resistant response to bradykinin. In fetal coronary arteries from nutrient-restricted ewes, relaxation to bradykinin was fully suppressed by NLA. Large-conductance, calcium-activated potassium channel (BKCa) currents did not differ in coronary smooth muscle cells from control and nutrient-restricted animals. The BKCa openers, BMS 191011 and NS1619, and 14,15-epoxyeicosatrienoic acid [a putative endothelium-derived hyperpolarizing factor (EDHF)] each caused fetal coronary artery relaxation and BKCa current activation that was unaffected by maternal nutrient restriction. Expression of BKCa-channel subunits did not differ in fetal coronary arteries from control or undernourished ewes. The results indicate that maternal undernutrition during pregnancy results in loss of the EDHF-like pathway in fetal coronary arteries in response to bradykinin, an effect that cannot be explained by a decreased number or activity of BKCa channels or by decreased sensitivity to mediators that activate BKCa channels in vascular smooth muscle cells. Under these conditions, bradykinin-induced relaxation is completely dependent on nitric oxide, which may represent an adaptive response to compensate for the absence of the EDHF-like pathway.
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