China
Africa
Explore chapters and articles related to this topic
Properties of the Arterial Wall
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Since the discovery of endothelium-derived relaxing factor (EDRF or nitric oxide [NO]) by Furchgott and Zawadzki (1980), it has become apparent that the endothelium plays a major role in modulation of vascular smooth muscle contraction and relaxation (Chapter 5) (Furchgott, 1983; Vanhoutte et al., 1986). Therefore, results from some earlier experiments on isolated specimens may be incorrect.
Microcirculation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The whole of the cardiovascular system (heart and blood vessels) is lined with a single layer of endothelial cells forming the surface in contact with blood. In addition to their functions of nutrient and waste product diffusion and fluid filtration, endothelial cells produce vasoactive substances throughout the cardiovascular system. Prostacyclin is produced by the endothelium from arachidonic acid, and it inhibits platelet adhesion and aggregation and vessel constriction. Endothelial cells generate the vasodilator nitric oxide (NO, endothelium-derived relaxing factor) from L-arginine. NO increases vascular smooth muscle cyclic guanosine monophosphate, which decreases intracellular calcium concentration, producing muscle relaxation and vasodilatation. Endothelial NO production is stimulated by acetylcholine, ATP, bradykinin, serotonin, substance P and histamine. NO production may also be enhanced by the effect on endothelial cell surface of the shear stress of blood flow. Endothelial cells also make the potent peptide vasoconstrictor endothelin, which increases peripheral vascular resistance and arterial blood pressure. Vascular endothelial cells, when stimulated by angiogenic factors, are able to form new capillary networks by cell division and movement.
Increased production of nitric oxide in cultured aortic smooth muscle cells from SHR
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Didier C. Junquero, Paul M. Vanhoutte
Furchgott and Zawadzky demonstrated the crucial role of the endothelial cells in the relaxations of isolated arteries evoked by acetylcholine (Furchgott and Zawadzki, 1980). Subsequently, several studies reported that vascular endothelial cells can regulate the tone of the smooth muscle layer by releasing both relaxing and contracting factors under basal conditions or after stimulation by neurotransmitters, hormones, autacoids or shear forces (Furchgott and Vanhoutte, 1989; Lüscher and Vanhoutte, 1990). Nitric oxide (NO), produced by the conversion of the terminal guanidino nitrogen atom(s) from L-arginine into L-citrulline, or a complex molecule yielding NO, accounts for many of the biological properties of endothelium-derived relaxing factor (EDRF)(Moncada et al., 1991). Endothelium-derived NO diffuses either toward the vascular lumen to prevent the activation and adhesion of platelets and neutrophils, or toward the underlying smooth muscle where it inhibits vascular tone. These effects evoked by NO are related to the activation of soluble guanylate cyclase leading to the accumulation of cyclic guanosine 3′, 5′-monophosphate (cyclic GMP) in target cells (Gruetter et al., 1981).
AChE mRNA expression as a possible novel biomarker for the diagnosis of coronary artery disease and Alzheimer’s disease, and its association with oxidative stress
Published in Archives of Physiology and Biochemistry, 2022
The AChE plays an important role in cholinergic metabolism by hydrolysing neurotransmitter acetylcholine (ACh) in cholinergic synapse (Aslan et al.2019, Türkeş et al.2019). Most of the ACh molecules released into the synaptic space bind to postsynaptic receptors. ACh molecules not bound to receptors are hydrolysed by AChE. According to the cholinergic hypothesis, there is a metabolic relationship between AD and CAD. The AChE, a cholinergic biomarker, also has an effect on coronary artery disease (CAD) as it hydrolyses ACh that provides flexibility within the blood vessels (Collins et al.1995). Endothelium-derived relaxing factor (EDRF), providing flexibility within the vessel, is provided by the vascular endothelium (Yanagisawa et al.1988, Rubanyi 1991). The EDRF is released by a number of physico-chemical stimuli, including ACh and endogenous hormones. The ACh stimulates endothelium-dependent relaxation in monkey, dog, rabbit, and human with CAD (Collins et al.1993).
Vasomotor tone-associated factors and pregnancy outcomes of women who undergo in vitro fertilization
Published in Growth Factors, 2021
Yonglian Lan, Xiaokui Yang, Yu Liang, Lingling Lei, Ying Li, Shuyu Wang
Nitric oxide (NO) is a well-known endothelium-derived relaxing factor involved in the control of vasomotor tone (Hull, White, and Pearce 1994). NO has been reported to be involved in the regulation of diverse reproductive processes, such as folliculogenesis, fertilization, ovarian blood flow, ovarian follicle maturation, and embryonic growth (Zhao et al. 2010; Lee et al. 2004). Some studies have also shown that high NO levels are related to poor outcomes of implantation. For example, the NO level in follicular fluid decreases with increasing follicle size (Kim et al. 2004). High follicular NO levels are associated with advanced fragmentation of embryos, and high serum NO levels are associated with implantation failure (Lee et al. 2004). Similar to NO, prostacyclin (prostaglandin I2 [PGI2]) is another vasodilator that contributes to the maintenance of vasomotor tone. The deficient intravascular production of PGI2 is closely associated with the occurrence of preeclampsia, hypertension, and abortion (Tulppala, Viinikka, and Ylikorkala 1991; Frölich 1990; Duley et al. 2019; Benigni and Remuzzi 2000). However, the specific roles of NO and PGI2 in the pregnancy outcome of IVF-ET have not been elucidated.
Investigating the role of nitric oxide in stress adaptive process in electric foot shock stress-subjected mice
Published in International Journal of Neuroscience, 2021
Rajdeep Kaur, Amteshwar Singh Jaggi, Anjana Bali
Nitric oxide (NO), an endothelium-derived relaxing factor, is generated from arginine in the presence of nitric oxide synthase enzymes and NO functions as a neurotransmitter as well as a neuromodulator [12]. Recent studies have demonstrated the potential role of NO in the stress and related disorders [13]. The increased mRNA and protein levels of neuronal nitric oxide synthase (nNOS) have been observed in the Paraventricular nucleus (PVN) of rats in response to stressful conditions [14,15]. The role of inducible NOS (iNOS) activity has also been implicated in the regulation of the HPA axis activation [16]. It has also been shown that NOS blockers inhibit immobilization stress-induced activation of c-fos in the PVN region [17] and attenuate immobilization stress-related anxiety response [18]. NO also modulates the release of various stress hormones including Corticotropin-releasing hormone (CRH), Adrenocorticotropic hormone (ACTH) and corticosterone [16,19–21], thus playing crucial role in regulating stress response [22].