Related Experiment Video

Updated: Apr 8, 2026

Author Spotlight: Traditional Chinese Medicine for Sleep Disorders in Acute COPD — A Safe, Cost-Effective Approach
04:53

Author Spotlight: Traditional Chinese Medicine for Sleep Disorders in Acute COPD — A Safe, Cost-Effective Approach

Published on: October 18, 2024

1.7K

Nocturnal hypoxemia severity and renin-angiotensin system activity in obstructive sleep apnea

Ann A Zalucky1, David D M Nicholl1, Patrick J Hanly1,2

  • 11 Department of Medicine.

American Journal of Respiratory and Critical Care Medicine
|June 24, 2015
PubMed
Abstract

Insights

The severity of nocturnal hypoxemia in obstructive sleep apnea (OSA) patients directly impacts kidney renin-angiotensin system (RAS) activation. This effect is independent of obesity, highlighting hypoxemia as a key factor in renal RAS activity.

Area of Science:

  • Nephrology
  • Sleep Medicine
  • Cardiovascular Physiology

Background:

  • Obstructive sleep apnea (OSA) and nocturnal hypoxemia are linked to chronic kidney disease and increased renin-angiotensin system (RAS) activity, potentially harming kidney function.
  • The specific influence of hypoxemia severity and obesity on RAS activation in OSA patients remains unclear.

Purpose of the Study:

  • To investigate the relationship between the severity of nocturnal hypoxemia and renal RAS activity in patients with OSA.
  • To determine if this association is independent of obesity in OSA patients.

Main Methods:

  • Measured effective renal plasma flow (ERPF) response to angiotensin II (AngII) challenge as a marker of renal RAS activity.
  • Utilized the para-aminohippurate clearance technique in 31 OSA subjects stratified by hypoxemia severity (moderate vs. severe) and 13 obese controls.

Main Results:

  • OSA patients exhibited reduced renovascular sensitivity to AngII compared to obese controls.
  • Severe nocturnal hypoxemia in OSA patients was associated with greater augmentation of renal RAS activity compared to moderate hypoxemia.
  • Hypoxemia severity did not correlate with blood pressure or systemic RAS component response to AngII.

Conclusions:

  • The severity of nocturnal hypoxemia significantly influences the degree of renal RAS activation in OSA patients.
  • This effect on renal RAS activity is independent of comorbid obesity.
  • Systemic RAS activation is not directly influenced by hypoxemia severity in this OSA cohort.
Keywords:
angiotensinhemodynamicshypoxemiakidneyobstructive sleep apnea

More Related Videos

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea07:54

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea

Published on: December 6, 2016

20.9K
A Model to Simulate Clinically Relevant Hypoxia in Humans09:54

A Model to Simulate Clinically Relevant Hypoxia in Humans

Published on: December 22, 2016

9.5K

Related Concept Videos

Sleep Apnea01:21

Sleep Apnea

Sleep apnea is a condition where breathing stops intermittently during sleep, often leading to significant health issues. Each episode can last from 10 to 20 seconds or more and is frequently accompanied by a brief arousal from sleep. This disturbance, largely unnoticed by the individual, can lead to severe daytime fatigue. Commonly, individuals seek help after being informed by their partners about loud snoring and noticeable breathing pauses during sleep.
The condition is more prevalent among...
786
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
1.5K
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
595
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
37.2K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.8K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.9K