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Transgenerational programming of the cardiovascular system by protein restriction in pregnancy
No full textEThOS - Electronic Theses Online ServiceGBUnited Kingdo
Transmission of raised blood pressure and endothelial dysfunction to the F2 generation induced by maternal protein restriction in the F0, in the absence of dietary challenge in the F1 generation
No full textWe have previously demonstrated that maternal protein restriction during pregnancy leads to raised blood pressure and endothelial dysfunction in the offspring (F1). Here we show that these characteristics are transmitted to the F2 offspring through the maternal line, in the absence of any additional challenges to the F1. Female Wistar rats were fed either a control (18 % casein) or protein-restricted diet (PR; 9 % casein) throughout pregnancy. Female F1 offspring, maintained on standard chow postpartum, were mated with breeding males to produce F2 progeny. Systolic blood pressure (SBP) in male F2 offspring was assessed by tail-cuff plethysmography at age 100 d and vascular function of small mesenteric arteries by wire myography at age 80 and 200 d. SBP was raised in PR F2 offspring compared with controls (control 122.1 (sem 2.3) mmHg, n 7; PR 134.7 (sem 3.2) mmHg, n 6; P < 0.01) and endothelial function, assessed by vasodilatation to acetylcholine, was impaired at both age 80 d (% maximal response: control 89.7 (sem 2.6), n 14; PR 72.7 (sem 4.4), n 15; P < 0.01) and 200 d (effective concentration equal to 50 % of maximum (pEC50): control 7.67 (sem 0.10), n 10; PR 7.33 (sem 0.07), n 8; P < 0.05). The present study demonstrates that both raised blood pressure and endothelial dysfunction are passed via the maternal line to grand-offspring in the absence of any additional dietary challenges to their F1 mothers. Risk factors for chronic disease may therefore be heritable by non-genomic processes
How to beet hypertension in pregnancy: is there more to beetroot juice than nitrate?
No full textPregnancy is associated with a number of structural and functional cardiovascular adaptations that ensure the fetus is adequately supplied with nutrients throughout all phases of growth and development. Failure to meet the increased metabolic demands can lead to significant maternal and fetal morbidity. Maternal hypertension, either pre-existing or developing during pregnancy, is complicated by the limitations of our current anti-hypertensive medication. The mainstays of anti-hypertensive treatment, such as angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor antagonists/blockers (ARBs/Sartans) and thiazide diuretics are associated with an increased risk of congenital abnormalities to the developing fetus (NICE, 2019). As such, there remains a need to increase the available options for treatment of hypertension in pregnancy
Developmental exposure to bisphenol A leads to cardiometabolic dysfunction in adult mouse offspring
No full textBisphenol A (BPA) is a chemical compound that has adverse health outcomes in adults when exposed during the perinatal period. However, its effect on cardiovascular function remains to be elucidated. In this study, we examined the effects of daily administration of BPA to pregnant mice from gestational days 11 to 19 on cardiometabolic outcomes in the adult offspring. Prenatal BPA exposure resulted in altered growth trajectory and organ size, increase adiposity and impaired glucose homeostasis in male and female offspring. In addition, these BPA offspring exhibited raised systolic blood pressure, and in the males this was accompanied by impaired vascular tone. The aortas in females, but not in males, from the BPA group also showed reduced estrogen receptor gene expression. These results indicate that prenatal exposure to BPA increased susceptibility of the offspring to developing cardiovascular and metabolic dysfunction later in lif
The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Resolvin E1, resolvin D1 and resolvin D2 inhibit constriction of rat thoracic aorta and human pulmonary artery induced by the thromboxane mimetic U46619
No full textBackground and Purpose: Omega-6 fatty acid-derived lipid mediators such as prostanoids, thromboxane and leukotrienes have well-established roles in regulating both inflammation and smooth muscle contractility. Resolvins are derived from omega-3 fatty acids and have important roles in promoting the resolution of inflammation, but their activity on smooth muscle contractility is unknown. We investigated whether resolvin E1 (RvE1), resolvin D1 (RvD1) and resolvin D2 (RvD2) can modulate contractions of isolated segments of rat thoracic aorta (RTA) or human pulmonary artery (HPA) induced by the α1-adrenoceptor agonist phenylephrine or the stable thromboxane A2 mimetic U46619.Experimental Approach: Contractile responses in RTA and HPA were measured using wire myography. Receptor expression was investigated by immunohistochemistry.Key Results: Constriction of RTA segments by U46619, but not by phenylephrine, was significantly inhibited by pretreatment for 1 or 24 hours with 10-100 nmol/L RvE1, RvD1 or RvD2. The inhibitory effect of RvE1 was partially blocked by a chemerin receptor antagonist (CCX832). RvE1 at only 1-10 nmol/L also significantly inhibited U46619-induced constriction of HPA segments, and the chemerin receptor, GPR32 and FPR2/ALX were identified in HPA smooth muscle.Conclusion and Implications: These data suggest that resolvins or their mimetics may prove useful novel therapeutics in diseases such as pulmonary arterial hypertension, which are characterised by increased thromboxane contractile activity. <br/
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