Angiotensin II Type 2 Receptor Provides an Endogenous Brake During Inflammation-Induced Microvascular Fluid Leak

Ereso, Alexander Q.; Ramírez, René; Sadjadi, Javid; Cripps, Michael W.; Cureton, Elizabeth L.; Curran, Brian; Victorino, Gregory P.

doi:10.1016/j.jamcollsurg.2007.07.026

Cited by 10 publications

(7 citation statements)

References 23 publications

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“…Because AngII downregulates ACE-2 expression, transition to a state of AngII deficiency is consistent with the increased ACE-2 expression noted at autopsy [10]. Of note, AngII reportedly increases microvascular permeability under basal conditions but decreases permeability during inflammation, an effect attributed to the inflammation-induced shift from type-1 to type-2 receptor expression [15].…”

Section: Vasculopathy and Dysregulated Inflammation In Covid-19supporting

confidence: 62%

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

2020

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Section: Vasculopathy and Dysregulated Inflammation In Covid-19supporting

confidence: 62%

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

2020

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“…28,30 Conversely, RAAS blockers cause balanced arterial and venous dilation, thus reducing the precapillary hydrostatic pressure, 30 and may also decrease capillary permeability, thus minimizing the shift of fluid to the interstitial compartment. [31][32][33] Peripheral edema rates among patients receiving CCB monotherapy in clinical trials vary, ranging from 7.5%-36.8%. 15,16,[34][35][36][37][38][39][40][41][42][43] Numerous studies have reported the incidence of peripheral edema in patients receiving combined treatment with a CCB and a RAAS inhibitor versus an alternate regimen (Table 3).…”

Section: Calcium Channel Blocker-induced Lower Extremity Edemamentioning

confidence: 99%

Managing Peripheral Edema in Patients With Arterial Hypertension

Epstein¹,

Roberts²

2009

American Journal of Therapeutics

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Calcium channel blockers (CCBs) play a vital role in the management of hypertension. Peripheral edema is the most common side effect reported with CCB monotherapy, especially with high-dose dihydropyridine CCBs. CCB-related peripheral edema is a dose-limiting effect that is usually medically benign but can compromise patient adherence. CCB-related peripheral edema may cause considerable discomfort and patient concern. Patients presenting with peripheral edema should undergo assessment for drug and nondrug causes. Rather than lowering the CCB dose or switching to another monotherapy, combination therapy (e.g, CCB plus a renin-angiotensin-aldosterone system inhibitor) can enhance blood pressure control, generally with lower doses of individual agents, and lessen the risk of adverse events. As recommended by consensus guidelines, addition of a renin-angiotensin-aldosterone system inhibitor as part of combination therapy may accelerate the time to goal blood pressure as well as help alleviate peripheral edema in affected patients. Successful management of CCB-related peripheral edema with lifestyle changes and rational combination therapy is likely to improve blood pressure control and patient outcomes.

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“…These recommendations are based on few data suggesting an increased risk of overall complication after RASi discontinuation [12, 13] in the perioperative setting, while intraoperative hypotension can be managed with available vasoactive drugs during anesthesia [14]. The RAS acts on the vascular function and promotes thrombosis [15–17]. Modulating the RAS is therefore likely to impact global outcome after major surgery.…”

Section: Introductionmentioning

confidence: 99%

Impact of renin-angiotensin system inhibitors continuation versus discontinuation on outcome after major surgery: protocol of a multicenter randomized, controlled trial (STOP-or-NOT trial)

Legrand

Futier²,

Léone

et al. 2019

Trials

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Background Chronic treatment of hypertension or heart failure very often includes an angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) as renin-angiotensin system inhibitors (RASi) treatments. To stop or not to stop these medications before major surgery remains an unresolved issue. The lack of evidence leads to conflicting guidelines with respect to RASi management before major surgery. The purpose of this study is to evaluate the impact of a strategy of RASi continuation or discontinuation on perioperative complications in patients undergoing major non-cardiac surgery. Methods This is a multicenter, open-labeled randomized controlled trial in > 30 French centers. In the experimental group, RASi will be continued while the treatment will be stopped 48 h before the surgery in the control arm. The primary endpoint is a composite endpoint of major complications after surgery. An endpoint adjudication committee will review clinical data and adjudicate efficacy endpoints while blinded to the assigned study drug group. Main analysis will be by intention-to-treat comparing the composite outcome measure at 28 days in the two groups. A total of 2222 patients are planned to detect an absolute complications difference of 5%. Discussion The results of the trial should provide robust evidence to anesthesiologists and surgeons regarding management of RASi before major non-cardiac surgery. Trial registration ClinicalTrials.gov, NCT03374449 . Registered on 11 December 2017. Electronic supplementary material The online version of this article (10.1186/s13063-019-3247-1) contains supplementary material, which is available to authorized users.

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Angiotensin II Type 2 Receptor Provides an Endogenous Brake During Inflammation-Induced Microvascular Fluid Leak

Cited by 10 publications

References 23 publications

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

Managing Peripheral Edema in Patients With Arterial Hypertension

Impact of renin-angiotensin system inhibitors continuation versus discontinuation on outcome after major surgery: protocol of a multicenter randomized, controlled trial (STOP-or-NOT trial)

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