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This mini-review focuses on recent topics on basic research in hypertension from the several points of view. The recent topics indicate that interorgan communication has received particular attention. Interresearcher communication and collaboration should also be further facilitated to truly understand the complex pathogenesis of hypertension and to develop the treatments.
Fructose might be a Clue to the Origin of Preeclampsia Insights from Nature and Evolution Preeclampsia is a hypertensive disorder of pregnancy. The pathogenesis remains unclear. Fructose has a critical role in fetal growth in early pregnancy, and might be a key role to developing preeclampsia. Here, we summarize the previous literatures regarding the physiological andpathological roles of fructose in pregnancy to propose studies to further investigate the pathogenesis of preeclampsia.
A mechanistic model on the epigenetics of exercise during pregnancy. Maternal exercise during pregnancy triggers hypermethylation and transcriptional suppression of the Agtr1a gene via increased DNMT1 and DNMT3B expression in MAs of SHR offspring. Downregulation of AT1R expression reduces the contribution of Ang II to vascular tone, ultimately improving vascular structure and function. VSMC vascular smooth muscle cell; Ang II angiotensin II; AT1aR angiotensin type 1 receptor (AT1R) alpha subtypes; Agtr1a AT1R alpha isoform gene; MAs mesenteric arteries; BP blood pressure.
The impact of intermittent hypoxia (1 min at 5% O2 and 5 min at 20% O2, 8 h/day) for 4 weeks (IH4W) in Ogt-Tg mice. Augmented O-GlcNAcylation may aggravate IH4W-induced right ventricular dysfunction and remodeling by promoting hypertrophy, mitophagy, and fibrosis via GSK-3β inactivation, increased p-Drp-1/MFN2 ratio, and Smad2 activation, respectively.
Arterial stiffness progresses with age and is associated with adverse cardiovascular disease events. Studies of associations between statin therapy and arterial stiffness have yielded mixed results. Multi-Ethnic Study of Atherosclerosis (MESA) participants (n = 1242) with statin medication use data at each exam and who had B-mode carotid ultrasound at baseline and Exam 5 after (mean ± [SD]) 9.4 ± 0.5 years were analyzed. Carotid arterial stiffness was measured using distensibility coefficient (DC) and Young’s elastic modulus (YEM). Statin therapy was noted to not be associated with changes in carotid artery stiffness over nearly a decade of follow up regardless of therapy duration or intensity.
Comparisons of the changes from baseline in vascular endothelial function parameters at 24 weeks among the 3 groups of low, moderae and high uric acid levels achieved with xanthine oxidase inhibitors. After adjustment for confounding factors, such as age, body mass index and concomitant diuretic use, which showed differences among the 3 groups, the change in RHI in the moderate uric acid level group tended to be higher than that in the high uric acid level group and was significantly higher than that in the low uric acid level group.
Accuracy of studied variables to predict masked hypertension in the derivation cohort. OBP – office BP; BMI – body mass index; DBP – diastolic BP; SBP – systolic BP; MH – masked hypertension; ESH – European Society of Hypertension; BSC – Brazilian Society of Cardiology; ACC/AHA – American College of Cardiology/American Heart Association
CV Cardiovascular, BP blood pressure. The diagram presents the groups of comparison, men versus women in hypertensive emergencies that completed the 1-year follow-up for outcomes, in terms of hospitalizations or deaths.