CardiologyTier 2Topic

Regulation of arterial blood pressure and the role of the renin–angiotensin–aldosterone system

Determinants of blood pressure

Arterial BP = cardiac output x systemic vascular resistance, regulated over different timescales by neural (seconds), hormonal (minutes-hours), and renal (hours-days) mechanisms
Understanding the layered timescale of BP regulation explains why different antihypertensive drug classes act on different parts of this system

Baroreflex (rapid, seconds) - carotid sinus/aortic arch baroreceptors -> medullary vasomotor centre -> autonomic adjustment of heart rate/contractility/vascular tone - buffers acute BP changes but resets over days, explaining why it does not prevent chronic hypertension
Renin-angiotensin-aldosterone system (RAAS) (minutes-hours) - the renal juxtaglomerular apparatus releases renin in response to reduced perfusion pressure, reduced Na+ delivery, or sympathetic activation -> angiotensin II (potent vasoconstrictor, stimulates aldosterone and ADH) -> aldosterone drives renal Na+/water retention -> sustained BP support
Renal pressure natriuresis (hours-days, the dominant long-term regulator) - rising BP directly increases renal Na+/water excretion, a negative feedback loop that ultimately sets the long-term BP "set point" - most chronic hypertension reflects a resetting of this renal mechanism, not a primary problem elsewhere

Explains the rationale for RAAS-blocking drugs (ACEi/ARB/MRA) as first-line antihypertensives - they interrupt the system most responsible for sustained BP elevation, not just acute regulation
Each RAAS component is a drug target: ACE inhibitors (block angiotensin II formation), ARBs (block the AT1 receptor), MRAs (block aldosterone's receptor) - see RAAS drug pharmacology

Essential hypertension, renal artery stenosis (activates RAAS via reduced perfusion pressure), primary hyperaldosteronism (autonomous aldosterone excess bypassing the normal renin-driven pathway)

The renal set-point model explains why most antihypertensive strategies ultimately work by shifting renal sodium handling, directly or indirectly

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