China
Africa
Explore chapters and articles related to this topic
Pulmonary Circulation
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
None of these agents are effective as treatment for systemic hypertension. The reason for the inefficacy of drug treatment in primary pulmonary hypertension (and in many other forms, particularly that associated with left-to-right shunts) may well be the structural nature of the obstructive defect in small blood vessels (Fishman, 1998). When fully established (Edwards, 1957; Sheehan et al., 2005), one sees plexiform lesions with thickened and thinned walls and a mixture of microaneurysms, microhemorrhage and thrombosis, similar to what are seen in the brain of elderly persons with dementia and stiffened arteries. This is discussed elsewhere (Chapter 14) and is attributed to high pulsatile energy loss in small blood vessels causing endothelial and medial damage. Endothelial damage is manifest as shedding of endothelial cells into the bloodstream. Severity and irreversibility of pulmonary hypertension in a congenital left-to-right shunt (in ventricular septal defect, patent ductus arteriosus etc.) can be gauged by a count of circulating endothelial cells (Smadja et al., 2009). Identification and early treatment of pulmonary hypertension may be of more importance than early treatment of systemic hypertension because elevation of pressure is of relatively greater magnitude and because secondary damage to blood vessels comes on more quickly. Early surgical treatment of congenital left to right shunts is the well-known and the accepted procedure to prevent development of pulmonary hypertension.
Satellite cells and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Neil R.W. Martin, Adam P. Sharples
Endothelial cells are found on the inner lining of blood vessels, including capillaries in skeletal muscle. Satellite cells are located near to capillaries, and as discussed earlier in the chapter, exercise brings satellite cells and capillaries into closer proximity (49). The interaction between endothelial cells and satellite cells appears to be important for regeneration and communication between satellite cells and endothelial cells may be important for satellite cell function.
Dopamine in the Immune and Hematopoietic Systems
Published in Nira Ben-Jonathan, Dopamine, 2020
Endothelial cells are squamous cells that line the interior surface of blood and lymphatic vessels, forming a monolayer interface between circulating blood or lymph in the lumen and the vessel wall. Cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells. Endothelium within the interior surfaces of the heart chambers is called endocardium. Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries.
Generation of a novel ex-vivo model to study re-endothelialization
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Siti Sarah Azman, Muhammad Dain Yazid, Nur Azurah Abdul Ghani, Raja Zahratul Azma Raja Sabudin, Mohd Ramzisham Abdul Rahman, Nadiah Sulaiman
Endothelial dysfunction begins with an initial injury or damage to the endothelial cells, which lead to changes in the endothelial function. These changes include impaired vasodilation, increased adhesion of leukocytes and platelets, increased vascular permeability and reduced production of nitric oxide [2]. In addition, the dysfunction triggers a phenotypic switch in SMC at the media layer leading to its proliferative state. The activated SMC start to proliferate and migrated to the intimal layer leading to IH, which results in the formation of a thickened neointima layer [7,8]. This condition contributes to the narrowing of the vessel lumen, leading to stenosis. The thickened intimal layer and altered vessel architecture due to IH can exacerbate endothelial dysfunction and perpetuate the cycle of vascular injury, inflammation and proliferation [9]. If the condition persists, it can lead to the development of several cardiovascular pathologies such as atherosclerosis, hypertension or vessel restenosis [10,11].
Folic acid enhances the cardiovascular protective effect of amlodipine in renal hypertensive rats with elevated homocysteine
Published in Clinical and Experimental Hypertension, 2023
Li Li, Xiaohui Tong, Zebin Ma, Lei Lv, Haipeng Liu, Guang Liang Chen
Endothelial cell dysfunction is an early indicator of atherosclerosis and vascular diseases. To evaluate endothelial cell function, plasma ET-1 and NO were measured. Plasma ET-1 was upregulated in 2K1C rats with HHcy, indicating endothelial cell dysfunction. Amlodipine significantly decreased the level of plasma ET-1, although the level was still significantly higher than that in normal rats. Notably, supplementation of FA (0.08 to 0.16âmg/kg/day) to amlodipine successfully reversed the augmented level of plasma ET-1 to that in normal rats (Figure 2c), but there is no difference between the amlodipine group and amlodipine-FA groups in ET-1. Hypertension plus HHcy also significantly decreased the level of plasma NO. Interestingly, FA individually and partly reversed the level of plasma NO, while amlodipine only exhibited a trend to upregulate it. FA supplementation to amlodipine at medium dosage showed further improvement in plasma NO compared to amlodipine or FA alone (Figure 2d).
FGFR2 modulates the Akt/Nrf2/ARE signaling pathway to improve angiotensin II-induced hypertension-related endothelial dysfunction
Published in Clinical and Experimental Hypertension, 2023
Kun Jiao, Ping Su, Yongling Li
Hypertension is a common chronic disease. Surveys show that the incidence of hypertension in developed countries such as Europe and the United States is as high as 20%, with clinical characteristics of elevated blood pressure and cardiac and cerebrovascular disease (13,14). However, the molecular mechanisms underlying its pathogenesis are unclear. As an important component of blood circulation and the immune system, vascular endothelial cells are involved in a wide range of biological processes, including the regulation of blood pressure, angiogenesis, fibrinolysis and inflammation (15,16). A previous study has shown that vascular endothelial cell dysfunction plays an important role in the occurrence and development of hypertension (17). Endothelial cells not only act as a physical barrier, but also secrete a variety of substances that affect contraction-relaxation function. Endothelial cell damage increases during hypertension (18). Therefore, the study of the molecular mechanism of vascular endothelial cells in the occurrence and development of hypertension is helpful to improve the level of diagnosis and treatment of hypertension. In this study, Ang II-induced HUVECs were used to simulate the hypertension model in vitro, and it was found that the viability was reduced while oxidative stress levels and apoptosis was increased of HUVECs induced by Ang II, which indicated that the model was successfully established.