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Antihypertensive Drug Classes
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Engi Abdel-Hady Algharably, Reinhold Kreutz
The core of the RAS pathway involves the conversion of angiotensinogen to angiotensin I (Ang I) by renin followed by its conversion to angiotensin II (Ang II) by ACE. Ang II acts via activation of angiotensin II receptor type 1 to induce arterial vasoconstriction, aldosterone synthesis and secretion, thus increasing sodium and water reabsorption and increasing blood pressure (BP) (3). ACE is also capable of degrading bradykinin (a potent vasodepressor peptide) which contributes to the increase in BP. ACE inhibitors inhibit competitively the activity of ACE resulting in downstream reduction of Ang II in blood and tissues as well as reduction of aldosterone secretion and stimulation of kallikrein-kinin system (1).
Impact of Dietary Polyphenols on Arterial Stiffness
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Tess De Bruyne, Lynn Roth, Harry Robberecht, Luc Pieters, Guido De Meyer, Nina Hermans
Endothelin-1 (ET-1), on the other hand, is a potent vasoconstrictor peptide with pro-oxidant and proinflammatory properties and is of interest in the development of endothelial dysfunction. ET-1 expression and production in endothelial cells is, among others, increased by Ang II-stimulation and ageing. ET-1 overexpression activates NADPH oxidase, and therefore ROS formation, causing oxidative stress and forming a positive feedback loop of oxidative stress-mediated endothelial oxidative injury and dysfunction. Next to that, oxidative stress also causes amplification of the angiotensin-converting enzyme (ACE) activity, subsequently stimulating the angiotensin II receptor type 1 (AT-1) receptor by Ang II, and thus inducing the production of ROS by NADPH oxidase and amplifying the detrimental process (Siti et al., 2015).
Hypertension and Obesity
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
RAAS components are not only present in WAT but also produced in the skeletal muscle, the liver, and the pancreatic islets, where they modulate insulin production from β-cells. In these key tissues for blood glucose control, RAAS governs a dual axis with opposing effects on glucose homeostasis. The angiotensin II receptor type 1 (AT1R) and aldosterone favor hyperglycemia and generate an increased diabetes risk. On the flip side, the angiotensin II receptor type 2 (AT2R) tends to lower blood glucose and protect against the risk of developing diabetes.
Combined effects of angiotensin receptor blocker use and physical training in hypertensive men
Published in Clinical and Experimental Hypertension, 2022
Tábata de Paula Facioli, Stella Vieira Philbois, Bruno Augusto Aguilar, Ana Catarine Veiga, Hugo Celso Dutra de Souza
Until recently, pharmacological therapeutic approaches were the only treatment methods used in clinical practice for decreasing the incidence of comorbidities and early mortality (4). Currently, angiotensin II receptor type 1 (AT1) receptor blockers are the preferred drugs for hypertension treatment. Studies have shown that these blockers increase spontaneous baroreflex sensitivity (BRS) and decrease cardiac sympathetic phasic influence, as assessed by HRV analysis (5,6). However, this finding is not corroborated by other authors, who have demonstrated that volunteers with SAH treated with AT1 receptor blockers or angiotensin-converting enzyme inhibitors did not show any alterations in cardiac autonomic modulation (5). While the effect of AT1 receptor blockers on BP reduction is undeniable, their effects on autonomic cardiovascular control are still conflicting, indicating the need for additional studies to confirm the positive effects of AT1 receptor blockers on autonomic cardiovascular control.
Chemical renal denervation-induced upregulation of the ACE2/Ang (1-7)/Mas axis attenuates blood pressure elevation in spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2020
Wenzheng Han, Ming Wang, Xinrong Zhai, Qian Gan, Shaofeng Guan, Xinkai Qu
Hypertension is a major risk factor for many cardiovascular diseases. Uncontrolled hypertension can damage target organs, including the heart, kidney, and brain. In many hypertension patients, blood pressure (BP) can be reduced by medicine, but in approximately 20–30% of hypertension patients, BP cannot be controlled by medicine. The renin-angiotensin system (RAS) is thought to play an important role in the pathogenesis of hypertension and other cardiovascular diseases (1). Inactive angiotensin (Ang) I can be cleaved to Ang II when catalyzed by angiotensin converting enzyme (ACE). Subsequently, the action of Ang II is mediated by two G protein-coupled receptors (GPCRs), namely, angiotensin II receptor type 1 (AT1) and type 2 (AT2). In this way, ACE, Ang II and the AT1 receptor (AT1 R) compose the ACE/Ang II/AT1 R axis of RAS (2,3). Traditionally, activation of the RAS is associated with elevated angiotensin (Ang) II levels which can induce vasoconstriction, inflammation, fibrosis and fluid retention (4). Based on this theory, ACE inhibitors (ACEIs) and AT1 receptor blockers (ARBs) are widely used to control hypertension.
Enhanced oral bioavailability of valsartan in rats using a supersaturable self-microemulsifying drug delivery system with P-glycoprotein inhibitors
Published in Pharmaceutical Development and Technology, 2020
Yoon Tae Goo, Seh Hyon Song, Dong Woo Yeom, Bo Ram Chae, Ho Yub Yoon, Chang Hyun Kim, Sun Young Park, Tae Hoon Kang, Sangkil Lee, Young Wook Choi
Valsartan (VST), an orally active non-peptide tetrazole derivative, selectively inhibits angiotensin II receptor type 1 (Flesch et al. 1997). It is widely used to treat hypertension and congestive heart failure (Park et al. 2016). VST exhibits poor solubility and low permeability in the gastrointestinal (GI) tract because of the two acidic moieties of the carboxylic acid and the tetrazole ring with pKa values of 3.9 and 4.7, respectively (Siddiqui et al. 2011; Nekkanti et al. 2016), thus resulting in relatively low oral bioavailability of approximately 23% in healthy subjects (Schmidt et al. 1998; Dixit et al. 2010). To enhance the solubility and GI absorption of VST, various formulation approaches, such as solid dispersion, spray-dried emulsion, supercritical antisolvent processes, and self-microemulsifying drug delivery systems (SMEDDSs), have been extensively studied (Yan et al. 2012; Baek et al. 2014; Kim and Baek 2014; Nekkanti et al. 2016).