Letter to the Editor
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Besides naloxone, the FDA-approved angiotensin II is potentially the antidote mechanistically for ACEI poisoning and overdose. (“Try Naloxone for Severe ACE Inhibitor Poisoning,” EMN. 2019;41:22; http://bit.ly/32qBZXz.) Although this is not on the label, the basic science of the renin-angiotensin-aldosterone system (RAAS) is well established in the literature. There are case reports of use specifically for ACEI OD and mixed antihypertensive ODs in the public domain now.
Hypotension from ACE inhibition reduces angiotensin II production, and causes angiotensin I build-up (as a substrate of ACE) and spillover into the RAAS nonclassical vasodilatory pathway (the reason ACEIs are so effective for hypertension). Replenishing angiotensin II restores the vasomotor tone (vasoconstrictor) and produces biofeedback at the juxtaglomerular apparatus to reduce renin secretion, decreasing the conversion of angiotensinogen to angiotensin I as well as angiotensin I cleavage and spillover into the nonclassical vasodilatory pathway while the ACEI onboard can metabolize. (J Emerg Med. 2019. pii: S0736-467930422In press; http://bit.ly/2kyx1b5.)
It's good to review the RAAS, so powerful and balanced for our hemodynamic stability.
Chris Galloway, MD
Castle Rock, CO