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Hypertension
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Hypertension begets hypertension (Byrom and Dodson, 1948; Pickering, 1968; Byrom, 1969; Ledingham, 1995). Elevated arterial pressure causes reactive vascular changes in the kidneys that have the effect of reducing renal blood flow and causing the release of renin, together with increased reabsorption of salt (Kaplan, 1992; Goldblatt, 1995). Renin catalyzes angiotensin I formation under the influence of angiotensin-converting enzyme (ACE). This forms angiotensin II, a potent vasoconstrictor and a stimulus for the production of aldosterone. The latter promotes further salt retention and increased blood volume. Hypertension creates a vicious circle, acutely and chronically. The vicious cycle was originally described by Byrom (1969) and is broken by modern therapies including especially those that target the renin-angiotensin-aldosterone axis.
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
RAAS is an essential part of blood pressure regulation. The system consists of enzymes and chemical messengers and involves multiple organs. The first step in RAAS is the liver’s production of angiotensinogen, which is converted by the enzyme renin into angiotensin I. This is the rate-limiting step in the RAAS system. Angiotensin I is then converted mostly in the lungs into angiotensin II by ACE. Angiotensin II has biological effects on blood pressure, including constriction of blood vessels, sodium and water retention by kidneys, and atherosclerotic changes to the vessels. The actions from angiotensin II stimulate the production of aldosterone in the adrenal glands. Aldosterone in turn also has blood pressure-related effects as it increases sodium and water retention by the kidneys. In addition to functioning at a multiorgan level, the RAAS system can also function at local organ levels, such as blood vessels and the heart.
Antioxidant Effects of Peptides
Published in Mesut Karahan, Synthetic Peptide Vaccine Models, 2021
Rümeysa Rabia Kocatürk, Fatmanur Zehra Zelka, Öznur Özge Özcan, Fadime Canbolat
Hypertension is a cardiovascular disease that affects approximately one quarter of the world’s population and is a controllable risk factor that plays a role in related complications. The angiotensin I-converting enzyme (ACE) is a dipeptityl carboxypeptitase and has the role of turning angiotensin I to angiotensin II. Angiotensin II has a general vasoconstriction impact. It plays an important physiological role in controlling blood pressure, liquid, and salt balance in vertebrates (Hartmann and Meisel 2007; Hayes et al. 2016) and peptides that repress the ACE enzyme are potentially assumed as agents that lower the blood pressure (Kannan, Hettiarachchy, and Marshall 2012). Therefore, a great deal of research has been carried out on the peptide production which shows antihypertensive activity from milk, cheese, meat, fish, and a wide variety of plants and algae. However, no correlation has been reported between in vivo antihypertensive effects and the results of in vitro studies investigating the inhibition of ACE enzymes. In this manner, there is no assurance that the result that is taken from ACE inhibition acquired in vitro will have a similar impact in vivo (Majumder and Wu 2013; Miralles, Amigo, and Recio 2018; Ünal, Şener, and Cemek 2018; Girija 2018).
Pharmacotherapy for hypertensive urgency and emergency in COVID-19 patients
Published in Expert Opinion on Pharmacotherapy, 2022
Fabio Angeli, Paolo Verdecchia, Gianpaolo Reboldi
Indeed, ACE2 receptors are regulators of the renin-angiotensin-aldosterone-system (RAAS) by catalyzing the cleavage of angiotensin I into angiotensin1-9, and angiotensin II into the vasodilator angiotensin1-7. Angiotensin II is a potent vasoconstrictor, a stimulant of aldosterone release, and a promoter of adverse reactions including hypercoagulability, endothelial dysfunction, enhanced inflammation, and increased oxidative stress. On the contrary, angiotensin1,7 exerts several protective cardiovascular effects by the inhibition of angiotensin II–induced signaling, vasodilatation, sympathetic modulation, and restoration of endothelial function [30,31]. Remarkably, the interaction between ACE2 and SARS-CoV-2 is associated with the phenomenon of ACE2 downregulation, with internalization of ACE2 receptors into cells [37,38] and consequent substantial loss of ACE2 receptor enzymatic activity from the external site of the membrane. These mechanisms lead to less angiotensin II inactivation and less generation of antiotensin1-7 (imbalance between angiotensin II overactivity and angiotensin1-7 deficiency) which may trigger inflammation, thrombosis, and, notably, a rise in BP (Figure 1) [30–32].
Renal and Hepatic Disease: Cnidoscolus aconitifolius as Diet Therapy Proposal for Prevention and Treatment
Published in Journal of the American College of Nutrition, 2021
Maria Lilibeth Manzanilla Valdez, Maira Rubi Segura Campos
Renin is a proteolytic enzyme that is synthesized in the kidney and participates in the renin–angiotensin–aldosterone cycle. This synthesis is responsible for changes in volume and pressure. Renin acts on the angiotensinogen that is released from the liver and when is coupled, angiotensin I is obtained. Subsequently, the pulmonary endothelium releases the angiotensin-converting enzyme, which synthesizes angiotensin II (Figure 2). Angiotensin II is responsible for vasoconstriction, through the mechanism of intracellular sodium retention, promoting the increase of serum osmolarity. Angiotensin II also stimulates the synthesis of aldosterone and stimulates proximal sodium reabsorption. This enzyme has two types of receptors I and II, the increase in angiotensin II concentrations and the increase of coupling to its receptors, produces a systemic vasoconstriction and increase in systemic arterial pressure, causing hypertension. Most of the pharmacological treatments block the type I receptors, these decrease the hypertension, by releasing nitric oxide and activating the tumor necrosis factor beta, which is an important pro-inflammatory factor (19).
Autophagy contributes to angiotensin II induced dysfunction of HUVECs
Published in Clinical and Experimental Hypertension, 2021
Di Liu, Wan-Pin Sun, Jing-Wei Chen, Yan Jiang, Rong Xue, Lin-Hui Wang, Koji Murao, Guo-Xing Zhang
Angiotensin II (Ang II) is one of the main components of the renin-angiotensin-aldosterone system and plays an important role in maintaining plasma sodium concentration, arterial blood pressure and extracellular volume. Over-secretion of Ang II results in an overwhelming number of chronic and acute diseases, such as hypertension, cell proliferation, inflammation, and fibrosis (1–3). Increasing number of investigation demonstrates the crucial role of Ang II in the development of cardiovascular diseases (4,5). Our previous studies have revealed that Ang II activates NADPH oxidase to increase the production of reactive oxygen species (ROS), leading to mitochondria release large amount of ROS, resulting in activation downstream signaling pathways (6,7), which subsequently has been confirmed by other investigators (8–10). Up to date, ROS has been demonstrated as one of the key regulators in mediating Ang II–induced tissue damage (11,12). Antioxidant therapy is now being supposed to as a supplement method in clinical patients with high Ang II level.