RAAS Dysregulation: Pathological Activation in Heart Failure and Hypertension

The renin-angiotensin-aldosterone system (RAAS) defends blood pressure and sodium balance. Juxtaglomerular cells in the kidney release renin when renal perfusion falls, when sympathetic activity rises or when less sodium reaches the macula densa. Renin converts angiotensinogen to angiotensin I, and angiotensin-converting enzyme (ACE) converts that to angiotensin II. Angiotensin II constricts arterioles and prompts the adrenal cortex to release aldosterone, which makes the kidney retain sodium and water and excrete potassium. After bleeding or dehydration this response protects the circulation. The clinical problem is a system that stays switched on when the circulation does not need rescuing: in heart failure, in hypertension and in kidney disease. Every drug turns the signal down at a different point, and each important adverse effect (low blood pressure, a rising creatinine, high potassium, angioedema) is a predictable result of turning it down. The nurse practitioner (NP) in Canada diagnoses, prescribes, adjusts doses and orders the monitoring tests within provincial scope. The lesson therefore follows the prescriber's decision at each result: which drug, what dose, what to recheck, and who receives the patient when the...