Bioresorbable coronary scaffolds in non-ST elevation acute coronary syndromes
Yoshinobu Onuma, Patrick W.J.C. Serruys in Bioresorbable Scaffolds, 2017
Vasomotion, mechanostransduction, adaptive shear stress, and the subsequent late luminal gain are all phenomena in which endothelial function is of paramount importance. From the functional perspective, the implantation of a metal-stent significantly limits these functions. In a recent study from our group, we quantified the in-scaffold vasomotor in response to three different doses of acetylcholine, which allowed us to document both endothelium-dependent vasodilation and spasm phenomena, and to nitroglycerin, an endothelium-independent vasodilator [35]. While acetylcholine responses are an accepted diagnostic and risk stratification tool [41], data on the functional normalization of vessels previously treated in the setting of an acute event have not been reported before. In our population, endothelium-dependent vasodilation was observed in about 30% of the subjects. Nitroglycerin-induced vasodilation was observed in about half of the lesions. Of note, these figures might further improve after further withdrawal of the scaffolding function of the BVS. Collectively, these data demonstrate functional normalization in a large fraction of the segments treated with a BVS already after 1 year.
Prediction of Dynamic Transcapillary Pressure Difference in the Coronary Circulation
Samuel Sideman, Rafael Beyar in Analysis and Simulation of the Cardiac System — Ischemia, 2020
There really is a question whether vasomotion is present in the coronary circulation. It was recently stated by Tomonek that the precapillary sphincters are not shown to be present, at least not convincingly, in the coronary system. Microcirculatory studies on other beds are normally done at very low oxygen consumption levels. The coronary bed is very active and may have a different regulatory mechanism. It is questionable whether one might state that if there is vasomotion in one organ, it has to be active in the heart as well.
Circulation of fluid between plasma, interstitium and lymph
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
Vasomotion is the cycling of arterioles between dilatation and constriction. In some tissues, such as skeletal muscle, vasomotion occurs rhythmically, several times per minute. Because capillary pressure depends partly on precapillar y resistance (Figure 11.4), each contraction phase reduces capillary pressure, allowing a transient absorption of interstitial fluid. Under these conditions the microcirculation alternates between states (a) and (b) in Figure 11.11, reducing the rate of lymph formation.
Role of P38 mitogen-activated protein kinase on Cx43 phosphorylation in cerebral vasospasm after subarachnoid hemorrhage
Published in International Journal of Neuroscience, 2019
Chao Lei, Yutian Ruan, Changcheng Cai, Bao He, Dong Zhao
It is widely accepted that CVS is a pathologic delayed and prolonged contraction of cerebral arteries which have been regarded as the disorder of cerebrovascular vasomotion, induced by a cascade activated by factors released into the subarachnoid space after SAH. Some data showed that vasomotion, the regular oscillations of vascular tone or diameter, require intercellular communication, and gap junction (GJ) channels are of key importance [7]. Gap junctions, through which signaling spreads along the cells in the vascular wall to coordinates the synchronized vasomotion of cerebrovascular, are known to clusters of intercellular channels consisting of connexins, with connexin 43 (Cx43) being the most abundant Cx within the vasculature and expressed in both endothelial and smooth muscle cells [8]. In our previous studies, we demonstrated that the alteration of Cx43 expression is closely related to CVS [9], and some studies showed that Cx43 expression upregulates CVS after SAH through a gap junctional intercellular communication (GJIC) dependent mechanism [10].
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
The endothelium is a single layer of cells that overlays the lumen of blood vessels and plays an important physiological role in vascular homeostasis. The endothelial cells integrate and modulate the fundamental functions of the vascular wall, which controls inflammation, coagulation, and thrombosis, as well as regulates vasomotion. Many of these functions are mediated through the release of nitric oxide (NO). Endothelial injury involves a complex pathophysiological process that includes both increased activation of endothelial cells and the initiation of endothelial dysfunction, leading to vascular damage in both metabolic and atherosclerotic diseases, including cardiovascular diseases, neurodegenerative disorders, pulmonary diseases, hypertension, renal diseases, cancer, and metabolic diseases (such as hyperglycemia or diabetes and hyperlipidemia) [10–12]. Taken together, endothelial cells mediate important physiological functions, including the maintenance of blood fluidity, modulation of vascular tone, regulation of inflammation and immune response, and management of oxidative stress and neovascularization.
Gut microbiota and hypertension: association, mechanisms and treatment
Published in Clinical and Experimental Hypertension, 2023
Zhihua Yang, Qingchun Wang, Yangxi Liu, Lin Wang, Zhao Ge, Zhenzhen Li, Shaoling Feng, Chongming Wu
The most important feature of endothelial dysfunction is the impair of vasomotor regulation. BA receptors such as nuclear receptor farnesoid X receptor (FXR) and membrane receptor G protein-coupled bile acid receptor-1 (GPBAR1) play important roles in regulating endothelial function (78,79). As endogenous vasodilators, BAs promote the production of NO and inhibit the release of Endothelin-1 (ET-1), thus regulating vasomotion and blood pressure (80). Renal-humor feedback is the main mechanism of long-term regulation of blood pressure. Abnormal renal function is a key factor in the pathogenesis of hypertension. In mice, deletion of FXR- or TGR5-related genes is associated with reduced expression of AQP-2 and impaired urine concentration (81), which impacts the development of hypertension. FXR and TGR5 are endogenous renal receptors. BAs can regulate renal pathophysiology by activating FXR, TGR5, and genes involved in inflammation and renal fibrosis (82). Furthermore, BA metabolism is closely related to the TMAO pathway. FXR regulates the activity of FMO3 (83). After entering the liver through the portal circulation, TMA will be oxidized into TMAO by liver FMO3. Afterward, TMAO enters the systemic circulation and promotes hypertension by altering lipid metabolism, platelet activity, and vascular promotion of AS (71). BAs can regulate lipid metabolism by activating FXR (84). Activation of TGR5 can reduce inflammation (85), promote insulin secretion, and improve insulin resistance, which in turn regulates the occurrence of hypertension (86).