Renin Angiotensin Aldosterone System

Also known as: RAAS

Schematic of the RAAS ©RVC 2008

Introduction

The RAAS is activated whenever blood flow through the kidneys is reduced and when there are sodium losses in conditions such as diarrhoes, vomiting or excessive sweating. These losses reduce extracellular fluid volume and this in turn reduces arterial blood pressure, which triggers the RAAS system through several different mechanisms.

RAAS Activation

The Mechanism Behind the RAAS

Summary of the purpose of the RAAS

In the event of blood pressure dropping Renin is secreted due to the decreased stretch of the juxtaglomerular cells and an increased sympathetic stimulation triggered by the decreased activation of arterial baroreceptors. This enzyme cleaves the alpha glycoprotein Angiotensinogen which is released from the liver. This produces Angiotensin 1 which is further converted by Angiotensin Converting Enzyme (ACE) to Angiotensin II mainly in the lungs but to a much lesser extent locally in the kidneys. Angiotensin 2 then works to restore blood pressure by inducing constriction of arterioles, which increases vascular resistance, and constricting veins which reduces vascular volume. In this section we cover its effects on and through the kidneys.

Effects of Angiotensin II on Blood Pressure

Angiotensin II acts on AT1 receptors to stimulate the release of aldosterone from the zona glomerulosa of the adrenal glands. This mineralocorticoid increases the reabsorption of sodium and therefore water and chloride from the distal tubule of the kidney, thus helping to increase blood pressure and volume. It also stimulates the thirst center and increases the secretion of anti-diuretic hormone (ADH) to help increase blood volume. The RAAS allows pressure to return to 50% of baseline within 15 minutes of a significant haemorrhage occuring.

Effects of Angiotensin II on GFR

If blood pressure drops then glomerular filtration rate (GFR) also drops due to a reduced blood flow through the kidneys. Therefore it is important to prevent this. If contraction of the efferent arteriole occurs then the pressure difference between the afferent and efferent arterioles increases creating a greater filtration pressure. This effect is mediated by Angiotensin II and means that when blood pressure falls there is minimum alteration of GFR. Blood flow which is already reduced due to the reduced pressure will then be further reduced by the increase in resistance. This increased renal resistance to blood flow and the maintained GFR has many advantageous effects.

Advantages of Constriction of the Efferent Arteriole

• If you increase the resistance in the kidneys you contribute to increasing total peripheral resistance. This helps to return blood pressure towards normal. (Angiotensin II also has vasoconstrictive effects in other organs.)
• The kidneys can tolerate the reduced perfusion allowing blood to be prioritised to organs which need it like the brain and heart.
• The constriction of the efferent arterioles also reduces hydrostatic pressure in the peritubular capillaries this increases reabsorption of water and salt thus helping to restore the ECF and thus helps to normalise blood pressure.
• The amount of waste excreted is variable with GFR. Thanks to the normalised GFR the excretion of waste products such as urea is maintained.

Effects of Angiotensin 2 On Sodium

• Induces insertion of Na⁺ channels into renal tubules via stimulation of AT₁ receptors
• Proximal tubule:
  • Apical - Na⁺/H⁺ exchangers
  • Basolateral Na⁺(HCO₃^-)₃ and Na⁺K⁺ATPase
• Thick ascending limb
  • Apical Na⁺/H⁺ exchangers and Na⁺K⁺2Cl^- symporter
• Collecting Duct
  • Epithelial Na⁺ channel
• Also stimulates Aldosterone

Revision

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