GLOSSARY

The renin–angiotensin–aldosterone system (RAAS) is a hormonal cascade that regulates blood pressure and body fluid volume by retaining sodium and water and constricting blood vessels. It is activated by low blood pressure, reduced blood volume and sodium deficit.

Steps of the Cascade

• Renin: secreted by the kidney’s juxtaglomerular cells.
• Angiotensinogen → angiotensin I: by the action of renin on liver-made angiotensinogen.
• Angiotensin I → angiotensin II: by the enzyme ACE, mainly in the lungs.
• Angiotensin II: vasoconstriction, stimulation of aldosterone release from the adrenal cortex, stimulation of thirst and ADH, and increased sodium reabsorption in the PCT.
• Aldosterone: increased sodium reabsorption and potassium excretion in the collecting duct.

Feedback

Rising pressure and blood volume and increased ANP inhibit renin release and switch off the system.

Clinical Importance

• Drugs: ACE inhibitors, ARBs, a direct renin inhibitor (aliskiren) and aldosterone antagonists (spironolactone) are among the most important drugs for high blood pressure, heart failure and kidney disease.
• Long-term overactivity: RAAS contributes to hypertrophy and fibrosis of the heart, vessels and kidney.

Relevance to Sport

• Activation during exercise: exercise, especially long and in the heat, activates RAAS through sympathetic stimulation and reduced kidney blood flow, helping conserve sodium and water.
• Heat acclimatisation: over 7–14 days of training in heat, increased aldosterone raises plasma volume by about 10–12 percent and lowers sweat sodium.
• Practical example: a football team preparing for a World Cup in a hot country benefits from RAAS adaptations that maintain blood volume and performance by doing 10–14 days of training in hot conditions before the tournament.