The renin-angiotensin-aldosterone system (RAAS) maintains long-term blood pressure primarily through which of the following mechanisms?

## RAAS and Long-Term Blood Pressure Regulation ### Overview **Key Point:** The RAAS is the primary long-term (hours to days) blood pressure regulation system. Unlike the baroreceptor reflex, which operates acutely, the RAAS works through fluid volume expansion and vasoconstriction. ### Mechanism of Action 1. **Trigger:** Decreased renal perfusion pressure or decreased plasma Na^+^ concentration 2. **Renin release:** Juxtaglomerular cells release renin 3. **Angiotensinogen → Angiotensin I:** Renin cleaves angiotensinogen (hepatic origin) 4. **Angiotensin I → Angiotensin II:** ACE (in lung endothelium) converts Ang I to Ang II 5. **Dual effects of Ang II:** - **Vasoconstriction:** Direct effect on vascular smooth muscle (immediate, minutes) - **Aldosterone secretion:** Stimulates adrenal cortex → ↑ Na^+^ and H~2~O reabsorption in collecting duct 6. **Volume expansion:** Increased blood volume → increased cardiac output → increased blood pressure ### RAAS vs. Baroreceptor Reflex | Feature | Baroreceptor | RAAS | |---------|--------------|------| | **Onset** | Seconds | Hours–days | | **Primary mechanism** | Neural (sympathetic/parasympathetic) | Hormonal (Ang II, aldosterone) | | **Main effect** | ↓ HR, ↓ contractility, vasodilation | ↑ Blood volume, vasoconstriction | | **Adaptation** | Yes (within days) | No (sustained) | | **Chronic HTN** | Not responsible | Major contributor | **High-Yield:** The RAAS is responsible for sustained hypertension in many pathological states (renal artery stenosis, primary hyperaldosteronism, chronic kidney disease). ACE inhibitors and ARBs block this system therapeutically. **Mnemonic:** **RAAS = Volume & Vasoconstriction** — Renin → Angiotensin II → Aldosterone → Sodium/water retention → Blood volume ↑ → BP ↑