RAAS to the Rescue: Angiotensin II for the Treatment of Vasodilatory Shock

Kyle Savio, Mercer University College of Pharmacy

Vasodilatory shock may be characterized as hypotension resulting from peripheral vasodilatation and poor response to vasopressor therapy. Sepsis is considered the main cause for vasodilatory shock by reducing the body’s ability to constrict blood vessels and maintain hemodynamics. Therapy has demonstrated reliance on adrenergic vasopressors such as norepinephrine, but these may fail in refractory vasodilatory shock. The renin-angiotensin-aldosterone system (RAAS) is noted to play an important role in preserving the vasculature to prevent vasodilatory shock. [1]

In vasodilatory shock, RAAS failure may present without a known mechanism. It is believed that the endothelial cells are blocked or hyperpolarized, preventing a response to angiotensin II. The lungs have demonstrated production and storage of angiotensin converting enzyme I and II which can limit effectiveness of RAAS in septic patients. Supplementing the body with angiotensin II may serve as therapy to reverse these vasodilatory effects. [2] Continue reading