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The Role of Flaxseed Micronutrients and Nitric Oxide (NO) in Blood Vessel and Heart Function
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
In brief, the renin-angiotensin-aldosterone system of the kidneys regulates blood volume. In response to rising blood pressure, the kidneys secrete renin into the blood. Renin converts the plasma protein angiotensinogen into angiotensin I, which in turn is converted into angiotensin II by enzymes from the lungs. Angiotensin II activates two mechanisms that raise blood pressure:
Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Renal artery stenosis: This reduces renal blood flow stimulating renin release and subsequent angiotensin II production. Angiotensin II causes hypertension by vasoconstriction and by stimulation of aldosterone release from the adrenal cortex, which promotes sodium retention by the kidney.
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.
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).
An evaluation of the fixed-dose combination sacubitril/valsartan for the treatment of arterial hypertension
Published in Expert Opinion on Pharmacotherapy, 2020
Markus Wehland, Ulf Simonsen, Niels Henrik Buus, Marcus Krüger, Daniela Grimm
Upon ingestion, LCZ696 dissociates into the two compounds, valsartan, and sacubitril. Valsartan is an angiotensin II receptor antagonist with high affinity (IC50 = 2.7 nmol/l) to the AT1 receptor [28]. The AT1 receptor is the most abundantly found angiotensin receptor in adults and has been localized in the kidney, the heart, vascular smooth muscle cells, the brain, the adrenal gland, platelets, adipocytes, and placenta. Practically all clinically meaningful effects of angiotensin II are mediated by the AT1 receptors, including vasoconstriction, sodium retention, increased endothelin secretion, vasopressin release, and elevated sympathetic activity, all leading to increased BP by either increased vascular tone or fluid retention [28]. By blocking angiotensin from binding to AT1, valsartan can effectively lower BP. Valsartan treatment increases plasma angiotensin II levels [29], which may lead to activation of cardioprotective AT2, Mas, and AT4 receptors [30] (Figure 2).
Acute restraint stress increases blood pressure and oxidative stress in the cardiorenal system of rats: a role for AT1 receptors
Published in Stress, 2020
Gabriel T. do Vale, Drieli Leoni, Arthur H. Sousa, Natália A. Gonzaga, Daniela L. Uliana, Davi C. La Gata, Leonardo B. Resstel, Cláudia M. Padovan, Carlos R. Tirapelli
Angiotensin II is described to play an important role in the development of some cardiovascular diseases including hypertension (Touyz et al., 2018). Most of the pathophysiological actions of this peptide in the cardiorenal system are mediated by AT1 receptors (Touyz & Schiffrin, 2000). In the kidney, cardiomyocytes and vascular smooth muscle cells AT1 receptors mediate fibrosis, lipoperoxidation, protein nitration, reduction of NO bioavalability and down regulation of antioxidant enzymes (Nguyen Dinh Cat, Montezano, Burger, & Touyz, 2013; Silva et al., 2017; Touyz & Schiffrin, 2000). AT1 receptors are coupled to various signaling molecules including the enzyme nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase (Touyz & Schiffrin, 2000). The latter is an enzymatic complex composed by seven distinctive catalytic subunits termed Nox1–5, Duox1 and Duox2. Members of the “Nox family” are capable of reducing O2 leading to the generation of superoxide anion (O2•−) (Rodiño-Janeiro et al., 2013). Hyperactivation of Noxes under pathological states contributes to oxidative stress and consequent cardiovascular and renal injury (Sedeek, Hébert, Kennedy, Burns, & Touyz, 2009).