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Occupational toxicology of the kidney
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
Glomerular blood pressure and blood flow is regulated by the afferent and efferent arterioles which are innervated by the sympathetic nervous system and also respond to angiotensin II, vasopressin, endothelin, prostanoids and cytokines. Glomerular filtration pressure is about 50 mmHg (75 mmHg of blood pressure minus an osmotic pressure of 25) which is sufficient to force a considerable fraction of blood plasma through the glomerulus with selective passage of water, electrolytes, low molecular weight proteins and other compounds, including waste products, into the filtrate.
Potential Targets for Imaging Atherosclerosis
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
David N. Smith, Mehran M. Sadeghi, Jeffrey R. Bender
Atherogenesis can begin early in life with EC activation (2). The pathological process is initiated by lipid deposition seen early in the subendothelial space with resultant inflammatory cell infiltration. In the presence of high circulating levels, LDL cholesterol is taken up by the endothelium. Passing through caveoli, LDL becomes trapped in the subendothelial extracellular space (3). This impairs the secretion of vasodilatory and anti-inflammatory factors, such as NO (4). The altered endothelium releases endothelin-1 (ET-1) and angiotensin II (ATII), which function as vasoconstrictors. This leads to VSMC hypertrophy and vascular remodeling (5,6). Circulating monocytes expressing type A scavenger receptors, which recognize acetylated LDL molecules, transmigrate through the endothelium to engulf the lipids within the subendothelial space. Monocytes differentiate into activated macrophages expressing higher levels of SR-A (7), CD 32 (8), SR-BI (9), CD68 (10), and the better-characterized CD36. CD36 activates the nuclear receptor peroxisome proliferator-activated receptor (PPAR)-gamma, a cell differentiating transcription factor. While PPAR-gamma is involved in induction of genes related to lipid metabolism, it also promotes the differentiation of monocytes to macrophages and foam cells upon oxidized LDL (oxLDL) exposure (11,12). Oxidized LDL is formed by active oxidases [e.g., metalloproteinases, xanthine and NAD(P)H oxidases] in the intimal layer from macrophages and EC (13). The intracellular accumulation of cholesterol overwhelms the mitochondrial metabolic capacity and endoplasmic reticulum membrane integrity leading to organelle dysfunction, cell activation and release of proinflammatory cytokines and proteases within the growing lesion. Excess reactive oxygen species generated by the metabolism of lipids are incompletely neutralized by natural antioxidants (e.g., NADPH) (14,15), leading to further EC damage.
Nanomedicinal Genetic Manipulation: Promising Strategy to Treat Some Genetic Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Biswajit Mukherjee, Iman Ehsan, Debasmita Dutta, Moumita Dhara, Lopamudra Dutta, Soma Sengupta
Macitentan and Ambrisentan are approved Endothelin A receptor (ETA) antagonist utilized for pulmonary hypertension, which prevents the binding of ET1 to both ETA and ETB (Paulis et al., 2015; Iglarz et al., 2008).
The vasorelaxant effect of Canarium odontophyllum Miq. (Dabai) extract in rat thoracic aorta
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Dayang Fredalina Basri, Nur Sa'adah Abdul Rahman, Shafreena Shaukat Ali, Satirah Zainalabidin
Vascular endothelium which is located between the circulating blood and vascular smooth muscle plays an important role in regulating the vascular tone. Modulation of vascular tone by endothelium is mediated by the release of vasodilators (NO and prostacyclin) and vasoconstrictors such as endothelin and angiotensin II [17]. Relaxation in vascular smooth muscle can occur through the NO/cGMP pathway. In endothelial cell, the calcium-calmodulin complex stimulates NO synthase (NOS), which later activates NO formation from L-Arginine. NO then enters the smooth muscle cells and stimulates guanylate cyclase, which increases intracellular cyclic guanosine monophosphate (cGMP). The increased of the intracellular cGMP then stimulate cGMP dependent protein kinases leading to a decrease in the calcium concentrations in the smooth muscle cells, which causes its relaxation [18].
Ginkgo biloba modulates ET-I/NO signalling in Lead Acetate induced rat model of endothelial dysfunction: Involvement of oxido-inflammatory mediators
Published in International Journal of Environmental Health Research, 2023
Jerome Ndudi Asiwe, Godwin D. Yovwin, Nwoke Enekabokom Ekene, Simon Irikefe Ovuakporaye, Anthony Chibuzor Nnamudi, Eze Kingsley Nwangwa
Abnormal functioning of endothelial nitric oxide synthase (eNOS), a vasoactive enzyme involve in the biosynthesis of nitric oxide (NO), an endothelial relaxing factor, have been shown to be among lead acetate induced endothelial toxicity mechanism (Guerby et al. 2021). NO is produced by the endothelial cells and induces vasorelaxation in vascular smooth muscle (Kudo et al. 2021). Adequate endothelial NO is required to maintain normal vascular physiology in the face of decreasing NO bioavailability. However, endothelial dysfunction is hypothesized to be connected to a decrease in NO bioavailability, which leads to increased vulnerability to vascular injuries (Akbar et al. 2021). Lead exposure lowered NO levels, indicating a problem with the vasorelaxation mechanism, while Ginkgo biloba treatment, on the other hand, restored NO levels. Additionally, changes in vasoactive hormones, calcium transport, and its intracellular distribution have been documented to accompany lead-induced endothelial dysfunction (Franzin et al. 2021). Endothelin-I (ET-1) is a powerful vasoconstrictor peptide that plays a major role in cardiovascular disease (CVD) regulation. Increased production of ROS due to lead exposure has been linked to elevated endothelial ET-I level or activity, which consequently results in eNOS uncoupling, reduced NO bioavailability, and endothelial dysfunction (Torres Crigna et al. 2021). NO’s ability to act as a pro-oxidant as well as antioxidant in disease and in health has been proven in a series of investigations spanning decades (Chazelas et al. 2021). According to reports, NO promotes overactivity of glutamate signalling as a feedback transmitter, which can contribute to excitotoxicity and peroxynitrite-induced oxidative damage (Pietrancosta et al. 2020). It is possible that the combined release of glutamate and tumor necrosis factor-alpha (TNF-α) in the endothelium creates a micro-environment that aggravates endothelial dysfunction (Vernazza et al. 2020). The interplay of NO and ET-1 signalling in the organism regulates blood pressure and vascular tone (Stanisic et al. 2021). Increased activity of ET-1 in rats may be linked to the lead acetate-induced reduction in NO level, disrupting the vasoconstriction and vasodilation delicate balance (Zhuang et al. 2022). Treatment with Ginkgo biloba, however, considerably lowered ET-1, which is an indication that the equilibrium between vasodilation and vasoconstriction has been restored and hence protection from lead-induced vascular dysfunction.