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The Treatment of Hypertension with Nutrition, Nutritional Supplements, Lifestyle and Pharmacologic Therapies
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
These abnormalities coexist and interact with genetics, epigenetics, nutrient-gene expression and other environmental and lifestyle factors [2–5,11–14]. Hypertension is the “correct” but chronic dysregulated response to numerous infinite insults to the endothelium with gene expression patterns in which the vascular system becomes an innocent bystander [2–5,11–14]. Hypertension is one of several responses of the blood vessel that include endothelial dysfunction (ED) and cardiac and vascular smooth muscle dysfunctions with abnormalities of both microvascular function and structure which may precede the development of hypertension by decades. These changes lead to vascular and cardiac hypertrophy, remodeling, functional and structural network rarefaction, decreased vasodilatory reserve, altered vascular media to lumen ratio (MLR), stiffness, loss of arterial elasticity, fibrosis, increased pulse pressure, elevated pulse-wave velocity (PWV) and increased augmentation index (AI) [2–5,11–14].
The Erythrocyte as a Cellular Model for the Clinical Investigation of Essential Hypertensive Patients
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
Antonio Coca, Ricardo P. Garay
In noradrenergic neurons and/or in cardiocytes, the high for the sodium pump may led to transitory increases in cell Na+ contents after the action potential. This in turn may increase noradrenergic and/or cardiac output. In vascular smooth muscle, the high Km for the calcium pump may induce a delayed recovery of basal cytosolic calcium levels after muscle contraction.
Microvascular Architecture and Networks
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
In view of the anatomical and topological characteristics of microvascular networks, it is almost surprising that, normally, tissue supply is remarkably well adapted to metabolic demand. According to the classical theory, this is due to the local control of vascular smooth muscle tone by mediator/metabolites released according to metabolic activity from the tissue cells. While this concept is still generally acceptable, it needs to be modified and complicated in view of the many observations demonstrating mechanisms that appear to act independently of local metabolic activity. Among these, endothelium-dependent, myogenic, and neurogenic mechanisms are particularly prominent. In addition, metabolic signals from the surrounding tissue will only be able to reach the intraparenchymal blood vessels, and even maximal dilatation of these vessels would not be sufficient to generate the maximal flow rates observed. It is therefore evident that: Mechanisms must be present whose integrating action leads to a coordinated response of complex microvascular units or networks.Mechanisms of communication along the vascular tree are required to allow for a response also of those upstream vessels that cannot be reached by intraparenchymal signals.
Gastrodin attenuates angiotensin II-induced vascular contraction and MLCK/p-MLC2 pathway activation
Published in Pharmaceutical Biology, 2023
Zhi Guo, Xuan Yang, Meizhu Wu, Aling Shen, Jiapeng Li, Xiuli Zhang, Ying Cheng, Qiurong Xie, Jun Peng
Abnormalities in vascular function and structure underlie the initiation and development of hypertension (Schiffrin 2012). Previous studies have revealed that gastrodin treatment has a protective effect on blood vessels in vascular dementia (Li et al. 2022) and diabetes-induced cerebellar alterations (Zhang et al. 2020). However, few studies have evaluated the effect of gastrodin on vascular structural changes and dysfunction caused by hypertension. The ultrasound and H&E staining results in the present study demonstrate that gastrodin treatment reduces the thickness and PWV of the abdominal aorta, indicating gastrodin reduces vascular pathological changes and dysfunction in hypertensive mice. In addition, augmented vasoconstriction is a pathological characteristic of hypertension, typically due to increased vasoconstriction mediated by vascular smooth muscle (Touyz et al. 2018). The identification of DETs and KEGG analysis following gastrodin treatment demonstrated enrichment of vascular smooth muscle contraction signalling pathways, highlighting the role of gastrodin treatment on vasoconstriction and vasorelaxation. Our ex vivo studies of vascular tension revealed that gastrodin causes vasorelaxation of abdominal aortic rings precontracted with NE and ameliorates Ang II-induced vasoconstriction, which corroborate previous studies reporting the vasorelaxant effect of gastrodin on isolated thoracic aorta rings (Xie et al. 2015) and mesenteric artery rings (Chen et al. 2017) in rats.
MicroRNA-144 silencing attenuates intimal hyperplasia by directly targeting PTEN
Published in Clinical and Experimental Hypertension, 2022
Vascular smooth muscle cells (VSMCs) within the middle layer of the vessel wall are not terminally differentiated that can alter their phenotype in response to changing local environmental cues, which the cellular transition is well recognized as phenotypic switching of VSMC (1). Specifically, the mature VSMCs show contractile or differentiated character with extremely low rates of proliferation and migration. Upon the various cellular stimuli, the differentiated VSMCs transform into a synthetic phenotype, characterized as increased rates of proliferation, migration, and synthesis of extracellular matrix components, as well as reduced expression of differentiation markers, including smooth muscle α-actin, smooth muscle 22α, and smooth muscle myosin heavy chain (2). Importantly, intimal hyperplasia contributed by VSMC phenotypic switching is the major cause of failure in atherosclerosis-related coronary heart diseases, followed by vascular revascularization therapy, including angioplasty, vascular stenting (3). However, the potential target and molecular mechanisms underlying VSMC phenotypic switching and intimal hyperplasia still need to be widely investigated. .
Different cardiovascular responses to exercise training in hypertensive women receiving β-blockers or angiotensin receptor blockers: A pilot study
Published in Clinical and Experimental Hypertension, 2022
Igor M. Mariano, Ana Luiza Amaral, Victor Hugo V. Carrijo, Juliene G. Costa, Mateus de L. Rodrigues, Thulio M. Cunha, Guilherme M. Puga
Moreover, reductions of BP variability after exercise training in populations with cardiovascular dysfunctions also appear to be promising (24,25) and their results can be independent of BP control (25). Thus, decreases found in SD24 and SDdn of SBP in the present study are consistent with literature. However, it should be noted that the majority of BP variability studies use aerobic training (24,26) and only few use combined exercise training (25). Besides that, not just the type, but the exercise intensity seems to be related to the BP variability in a bell-shaped relationship with the best results in moderate intensities (16). Its effect pathway seems to be more influenced by endothelium and vascular smooth muscle adaptations to training than of sympathetic vasomotor activity variations (16). The primary role of vessels is also reaffirmed by the consistent results of improvements by pharmacological interventions on BP variability after the use of calcium channel blockers (27–29) for causing significant improvements in vascular compliance by vasodilation (28).