Obstructive Sleep Apnea And The Vascular Renin Angiotensin System In Humans

2012 ◽  
Author(s):  
David D.M. Nicholl ◽  
Patrick Hanly ◽  
George Handley ◽  
Brenda Hemmelgarn ◽  
Marc Poulin ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Obstructive Sleep

scholarly journals Sex differences in renal hemodynamics and renin-angiotensin system activity post-CPAP therapy in humans with obstructive sleep apnea

2020 ◽  
Vol 318 (1) ◽  
pp. F25-F34 ◽  
Author(s):  
David D. M. Nicholl ◽  
Patrick J. Hanly ◽  
Ann A. Zalucky ◽  
George B. Handley ◽  
Darlene Y. Sola ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sex Differences ◽  
Sleep Apnea ◽  
Renin Angiotensin System ◽  
Renal Hemodynamics ◽  
Ang Ii ◽  
Cpap Therapy ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Obstructive Sleep

Men have faster loss of kidney function and greater renal renin-angiotensin system (RAS) activity compared with women. Obstructive sleep apnea (OSA) is common in chronic kidney disease; the vascular effects of OSA differ by sex, and OSA-associated glomerular hyperfiltration can be reversed by continuous positive airway pressure (CPAP) therapy. We evaluated sex differences in the effect of CPAP on renal hemodynamics and the renal RAS in OSA. Twenty-nine Na+-replete, otherwise healthy study participants with OSA (10 women and 19 men) with nocturnal hypoxemia were studied pre- and post-CPAP (>4 h/night for 4 wk). Renal hemodynamics [renal plasma flow (RPF), glomerular filtration rate (GFR), and filtration fraction(FF)] were measured at baseline and in response to ANG II challenge, as a marker of renal RAS activity, pre- and post-CPAP therapy for 1 mo. In women, CPAP was associated with increased RPF (626 ± 22 vs. 718 ± 43 mL/min, P = 0.007, pre- vs. post-CPAP), maintained GFR (108 ± 2 vs. 105 ± 3 mL/min, P = 0.8), and reduced FF (17.4 ± 0.8% vs. 15.0 ± 0.7%, P = 0.017). In men, CPAP was associated with maintained RPF (710 ± 37 vs. 756 ± 38 mL/min, P = 0.1), maintained GFR (124 ± 8 vs. 113 ± 6 mL/min, P = 0.055), and reduced FF (18.6 ± 1.7% vs. 15.5 ± 1.1%, P = 0.035). Pre-CPAP, there were no sex differences in renal hemodynamic responses to ANG II. CPAP use was associated with a greater renovasoconstrictive response to ANG II in women (RPF at Δ30 min: −100 ± 27 vs. −161 ± 25 mL/min, P = 0.007, and RPF at Δ60 min: −138 ± 27 vs. −206 ± 32 mL/min, P = 0.007) but not men. CPAP use was associated with improved renal hemodynamics in both sexes and downregulated renal RAS activity in women but not men.

scholarly journals CPAP Therapy Delays Cardiovagal Reactivation and Decreases Arterial Renin-Angiotensin System Activity in Humans With Obstructive Sleep Apnea

2018 ◽  
Vol 14 (09) ◽  
pp. 1509-1520 ◽  
Author(s):  
David D.M. Nicholl ◽  
Patrick J. Hanly ◽  
Ann A. Zalucky ◽  
Michelle C. Mann ◽  
Jennifer M. MacRae ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Renin Angiotensin System ◽  
Cpap Therapy ◽  
Angiotensin System ◽  
System Activity ◽  
Renin Angiotensin ◽  
Obstructive Sleep

Nocturnal Hypoxemia Severity and Renin–Angiotensin System Activity in Obstructive Sleep Apnea

2015 ◽  
Vol 192 (7) ◽  
pp. 873-880 ◽  
Author(s):  
Ann A. Zalucky ◽  
David D. M. Nicholl ◽  
Patrick J. Hanly ◽  
Marc J. Poulin ◽  
Tanvir C. Turin ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
System Activity ◽  
Renin Angiotensin ◽  
Nocturnal Hypoxemia ◽  
Obstructive Sleep

Role of angiotensin II in chronic intermittent hypoxia-induced hypertension and cognitive decline

2021 ◽  
Vol 320 (4) ◽  
pp. R519-R525
Author(s):  
Alexandria B. Marciante ◽  
Brent Shell ◽  
George E. Farmer ◽  
J. Thomas Cunningham
Keyword(s):  
Sleep Apnea ◽  
Cognitive Decline ◽  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Common Mechanism ◽  
Chronic Intermittent Hypoxia ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Increase Risk ◽  
Subsequent Activation

Sleep apnea is characterized by momentary interruptions in normal respiration and leads to periods of decreased oxygen, or intermittent hypoxia. Chronic intermittent hypoxia is a model of the hypoxemia associated with sleep apnea and results in a sustained hypertension that is maintained during normoxia. Adaptations of the carotid body and activation of the renin-angiotensin system may contribute to the development of hypertension associated with chronic intermittent hypoxia. The subsequent activation of the brain renin-angiotensin system may produce changes in sympathetic regulatory neural networks that support the maintenance of the hypertension associated with intermittent hypoxia. Hypertension and sleep apnea not only increase risk for cardiovascular disease but are also risk factors for cognitive decline and Alzheimer’s disease. Activation of the angiotensin system could be a common mechanism that links these disorders.

Invited Review: Physiological consequences of intermittent hypoxia: systemic blood pressure

2001 ◽  
Vol 90 (4) ◽  
pp. 1600-1605 ◽  
Author(s):  
Eugene C. Fletcher
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Intermittent Hypoxia ◽  
Cardiovascular Response ◽  
Acute Hypoxia ◽  
Renin Angiotensin System ◽  
Systemic Blood Pressure ◽  
Angiotensin Ii Receptor ◽  
Obstructive Sleep

One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.

Nocturnal hypoxemia severity influences the effect of CPAP therapy on renal renin-angiotensin-aldosterone system activity in humans with obstructive sleep apnea

SLEEP ◽  
2020 ◽  
Author(s):  
David D M Nicholl ◽  
Patrick J Hanly ◽  
Ann A Zalucky ◽  
George B Handley ◽  
Darlene Y Sola ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Angiotensin Ii ◽  
Renal Hemodynamics ◽  
Cpap Therapy ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Nocturnal Hypoxemia ◽  
Obstructive Sleep ◽  
The Impact

Abstract Study Objectives Nocturnal hypoxemia (NH) in obstructive sleep apnea (OSA) is associated with renal renin-angiotensin-aldosterone system (RAAS) up-regulation and loss of kidney function. Continuous positive airway pressure (CPAP) therapy is associated with RAAS down-regulation, though the impact of NH severity remains unknown. We sought to determine whether NH severity alters the effect of CPAP on renal hemodynamics and RAAS activity in humans. Methods Thirty sodium-replete, otherwise healthy, OSA participants (oxygen desaturation index ≥15h -1) with NH (SpO2<90%≥12%/night) were studied pre- and post-CPAP (>4h/night∙4wks). NH severity was characterized as moderate (mean SpO2[MSpO2]≥90%; N=15) or severe (MSpO2<90%; N=15). Glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) were measured at baseline and in response to Angiotensin-II (3ng/kg/min∙30min, 6ng/kg/min∙30min), a marker of RAAS activity. Results Pre-CPAP, baseline renal hemodynamics did not differ by NH severity. Pre-CPAP, severe NH participants demonstrated blunted GFR (Δ30min, -9±4 vs 1±3mL/min, p=0.021; Δ60min, -5±5 vs 8±5mL/min, p=0.017) and RPF (Δ30min, -165±13 vs -93±19mL/min, p=0.003; Δ60min, -208±18 vs -112±22mL/min, p=0.001; moderate vs severe) responses to Angiotensin-II. Post-CPAP, severe NH participants demonstrated maintained GFR (112±5 vs 108±3mL/min, p=0.9), increased RPF (664±35 vs 745±34mL/min, p=0.009), reduced FF (17.6±1.4 vs 14.9±0.6%, p=0.009), and augmented RPF responses to Angiotensin-II (Δ30min, -93±19 vs -138±16mL/min, p=0.009; Δ60min, -112±22 vs -175±20mL/min, p=0.001; pre- vs post-CPAP), while moderate participants were unchanged. Conclusions Correction of severe, but not moderate, NH with CPAP therapy was associated with improved renal hemodynamics and decreased renal RAAS activity in humans with OSA.

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