A Potential Role of the Renin-Angiotensin-System for Disturbances of Respiratory Chemosensitivity in Acute Respiratory Distress Syndrome and Severe Acute Respiratory Syndrome
Open Access
- 20 January 2021
- journal article
- research article
- Published by Frontiers Media SA in Frontiers in Physiology
Abstract
Acute respiratory distress syndrome (ARDS) represents an acute diffuse inflammation of the lungs triggered by different causes, uniformly leading to a noncardiogenic pulmonary edema with inhomogeneous densities in lung X-ray and lung CT scan and acute hypoxemia. Edema formation results in “heavy” lungs, inducing loss of compliance and the need to spend more energy to “move” the lungs. Consequently, an ARDS patient, as long as the patient is breathing spontaneously, has an increased respiratory drive to ensure adequate oxygenation and CO2 removal. One would expect that, once the blood gases get back to “physiological” values, the respiratory drive would normalize and the breathing effort return to its initial status. However, in many ARDS patients, this is not the case; their respiratory drive appears to be upregulated and fully or at least partially detached from the blood gas status. Strikingly, similar alteration of the respiratory drive can be seen in patients suffering from SARS, especially SARS-Covid-19. We hypothesize that alterations of the renin-angiotensin-system (RAS) related to the pathophysiology of ARDS and SARS are involved in this dysregulation of chemosensitive control of breathing.This publication has 115 references indexed in Scilit:
- Acute respiratory distress syndrome leads to reduced ratio of ACE/ACE2 activities and is prevented by angiotensin‐(1–7) or an angiotensin II receptor antagonistThe Journal of Pathology, 2011
- Angiotensin and carotid body chemoreception in heart failureCurrent Opinion in Pharmacology, 2011
- Astrocytes Control Breathing Through pH-Dependent Release of ATPScience, 2010
- Animal models of acute lung injuryAmerican Journal of Physiology-Lung Cellular and Molecular Physiology, 2008
- Angiotensin converting enzyme-2 is protective but downregulated in human and experimental lung fibrosisAmerican Journal of Physiology-Lung Cellular and Molecular Physiology, 2008
- Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal CordJournal of Neuroscience, 2008
- The discovery of angiotensin‐converting enzyme 2 and its role in acute lung injury in miceExperimental Physiology, 2008
- Lethal Infection of K18- hACE2 Mice Infected with Severe Acute Respiratory Syndrome CoronavirusJournal of Virology, 2007
- Differential expression of neuronal ACE2 in transgenic mice with overexpression of the brain renin-angiotensin systemAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2007
- An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels.JCI Insight, 1990