Overactivity of the renin-angiotensin-aldosterone system (RAAS) is a consistent feature of COVID-19 as indicated by high concentrations of angiotensin II (Ang II) in lungs and other tissues. Virus-induced downregulation of angiotensin-converting enzyme-2 (ACE2) explains the raised Ang II levels. Available evidence points to the crucial role of Ang II in the pathogenesis of coronavirus disease. The proinflammatory, immune stimulant, and procoagulant effects exhibited by the peptide at high tissue levels explain lung injury, a characteristic feature of severe COVID-19. Angiotensin II (Ang II) inhibitors [both the angiotensin-converting enzyme inhibitors (ACEIs) and the angiotensin receptor blockers (ARBs)] constitute the logical therapy for established COVID-19 infection. While ACEIs help to lower Ang II levels in the tissues, ARBs antagonize the effects of the peptide on the target tissues. Of the two, ARBs offer a better choice because of the minimal adverse effects of dry cough and angioedema. The effectiveness of Ang II inhibitors in COVID-19 is well supported by their protective effect against lung injury in animals induced by the virus spike protein as well as the clinical improvement of shortened hospital stay and reduced mortality in observational studies in humans. A unique feature of these agents is that mutations of the coronavirus 2 (CoV-2) would have little impact on their effectiveness since they do not interfere with the host cell entry of the virus or its replication. Expectedly, the agents might retain their usefulness against variant strains, including "ο" and its subvariants. The overall safety of Ang II inhibitors has been well established beyond doubt since they have been in use for years in the management of cardiovascular (CV) diseases, diabetes mellitus, and chronic kidney disease (CKD). Regular use of ARBs in all patients who are COVID-19 positive and symptomatic (mild, moderate, or severe) offers a good option worth serious consideration. : S HT. COVID-19 Therapeutics Why Not Angiotensin Receptor Blockers (ARBs)? J Assoc Physicians India 2023;71(11):71-75.
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http://dx.doi.org/10.59556/japi.71.0393 | DOI Listing |
Sci Rep
December 2024
Department of Anatomy, Faculty of Science, Mahidol University, 272 Rama VI Road, Ratchathewi, Bangkok, 10400, Thailand.
SARS-CoV-2, the cause of COVID-19, primarily targets lung tissue, leading to pneumonia and lung injury. The spike protein of this virus binds to the common receptor on susceptible tissues and cells called the angiotensin-converting enzyme-2 (ACE2) of the angiotensin (ANG) system. In this study, we produced chimeric Macrobrachium rosenbergii nodavirus virus-like particles, presenting a short peptide ligand (ACE2tp), based on angiotensin-II (ANG II), on their outer surfaces to allow them to specifically bind to ACE2-overexpressing cells called ACE2tp-MrNV-VLPs.
View Article and Find Full Text PDFNeuropharmacology
December 2024
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, ul. Mickiewicza 2A, 15-222 Białystok, Poland.
Although angiotensin 1-7 (Ang 1-7) and its role as a part of the "protective" axis of the renin-angiotensin system are well described in the literature, the mechanisms of its angiotensin II-like pressor and tachycardic effects following its acute central administration are not fully understood. It was the aim of the present study to examine which receptors contribute to the aforementioned cardiovascular effects. Ang 1-7 and antagonists for glutamate, GABA, vasopressin, thromboxane A (TP), α-adrenergic, and P2X purinoceptors or modulators of oxidative stress were injected into the paraventricular nucleus of the hypothalamus (PVN) of urethane-anesthetized male Wistar rats.
View Article and Find Full Text PDFPeptides
December 2024
Translational Medicine Centre, Jiangxi University of Chinese Medicine, Nanchang 330004, China. Electronic address:
Increasing evidence has demonstrated that sPRR [a truncated soluble form of (pro)renin receptor] levels may reflect the severity of several diseases, including kidney disease, hypertension, and heart failure (HF). Although previous studies using cohorts primarily consisting of HF patients with reduced ejection fraction revealed that increased plasma sPRR levels may be a promising evaluative indicator for HF, definitive information on the relationship between plasma sPRR levels and HF patients with preserved ejection fraction (HFpEF) is still insufficient and scarce. In the present study, we further clarified the status of plasma sPRR levels in HF patients by meta-analysis.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
October 2024
Department of Endocrinology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Sodium-glucose cotransporter 2 inhibitors (SGLT2Is) and angiotensin receptor-neprilysin inhibitor (ARNI) may cause potential renal damage, the combined impact of SGLT2Is and ARNI on acute kidney injury (AKI) remains unclear. This pharmacovigilance study conducted a disproportionality analysis using reports from the FAERS database. The reporting odds ratio (ROR) was used as an estimate for detecting AKI signal.
View Article and Find Full Text PDFOsteoporos Int
December 2024
Department of Cardiology, Chi-Mei Medical Center, Tainan, Taiwan.
Unlabelled: This study examined the impact of thiazide and RAAS antihypertensive medications vs DHP-RAAS medications on fracture risk. The close alignment of such settings with clinical use, combined with the potential bone benefits of ACEis and ARBs, provides enhanced accuracy in bone health evidence.
Purpose: To determine whether thiazides, combined with either angiotensin-converting enzyme inhibitor (ACEi) or angiotensin II receptor blocker (ARB), offer bone-protective benefits compared with dihydropyridine (DHP) drugs combined with ACEi or ARB.
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