Renin angiotensin system in BP regulation flow chart

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Renin-Angiotensin System in Blood Pressure Regulation

Overview Flow Chart (Robbins & Kumar Basic Pathology, Fig. 8.3)

This classic diagram shows how low BP triggers the RAAS cascade (right side raises BP) and how high BP triggers natriuretic peptides to lower it (left side lowers BP).

Full Molecular Pathway (Katzung Basic & Clinical Pharmacology, Fig. 17-3)

This diagram shows both the classical pathway (black) and the newer counter-regulatory pathways (blue = ANG 1-7/Mas receptor; red = prorenin receptor).

Step-by-Step Flow of the Classical RAAS

↓ Blood Pressure / ↓ Renal Perfusion / ↓ Renal Na⁺
            ↓
  Juxtaglomerular (JG) cells of kidney
  → Release RENIN
  (also triggered by: β1-adrenergic stimulation, PGE2;
   inhibited by: ANG II feedback, high Ca²⁺, ANP)
            ↓
  ANGIOTENSINOGEN (α-globulin, made in liver)
  ──[Renin cleaves]──→ ANGIOTENSIN I (10 aa, inactive)
            ↓
  ACE (Angiotensin-Converting Enzyme)
  — expressed on vascular endothelium, especially lungs —
  ──[ACE cleaves 2 aa]──→ ANGIOTENSIN II (8 aa, highly active)
            ↓
       AT₁ Receptors
      ↙              ↘
VASOCONSTRICTION    ADRENAL CORTEX
(arteriolar SMC)     → Aldosterone secretion
↑ Peripheral         → ↑ Na⁺ & H₂O reabsorption
  resistance           in distal tubule/collecting duct
                     → ↑ Blood volume
            ↓                  ↓
     ↑ BLOOD PRESSURE ←────────┘

Three Mechanisms by Which Ang II Raises BP

Mechanism	Target	Effect	Timing
Direct vasoconstriction	Arteriolar smooth muscle (AT₁)	↑ Peripheral resistance	Rapid (10-15 sec)
Aldosterone release	Adrenal zona glomerulosa	↑ Na⁺/H₂O retention → ↑ blood volume	Slow (hours-days)
Direct renal effect	Tubular cells + efferent arteriole constriction	↑ Na⁺/H₂O reabsorption, ↓ peritubular capillary pressure	Intermediate

Ang II is ~40× more potent than norepinephrine on a molar basis. The vasoconstrictor response takes ~20 minutes to become fully active - slower than baroreceptor reflexes but more sustained. - Katzung, Basic & Clinical Pharmacology 16e

Counter-Regulatory (Protective) Arm

The system has a built-in counter-balance:

ACE2 converts ANG I → ANG 1-9, and ANG II → ANG 1-7
ANG 1-7 acts on the Mas receptor → vasodilation, anti-inflammatory, anti-proliferative
This opposes AT₁-mediated effects and limits excessive vasoconstriction
ANP/BNP (released from cardiac volume sensors when BP is high):
- Cause natriuresis/diuresis → ↓ blood volume
- Cause vasodilation
- Directly inhibit renin release

Triggers for Renin Release (Stimuli)

Low renal artery pressure - JG cells sense stretch; hypotension = less stretch = more renin
Low tubular Na⁺ at macula densa - detected when GFR falls (e.g., heart failure)
Sympathetic activation - norepinephrine via β₁-adrenoceptors on JG cells (links stress/volume loss to RAAS)
Prostaglandins (PGE₂) - paracrine stimulation

Inhibitors of Renin Release

ANG II (short-loop negative feedback via AT₁)
High renal perfusion pressure (stretch)
ANP/BNP
High Na⁺ at macula densa

Drug Targets in the RAAS

Drug Class	Site of Action	Example
Direct renin inhibitors	Block renin	Aliskiren
ACE inhibitors	Block ACE	Enalapril, Lisinopril
ARBs	Block AT₁ receptor	Losartan, Valsartan
Aldosterone antagonists	Block aldosterone effect	Spironolactone
β-blockers	Reduce renin release (β₁)	Metoprolol

Sources:

Robbins & Kumar Basic Pathology, Fig. 8.3 - BP regulation interplay
Guyton and Hall Textbook of Medical Physiology - Chapter 19, RAS in arterial pressure control
Katzung Basic & Clinical Pharmacology 16e - Chapter 17, Renin-Angiotensin System

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