Describe the activation sequence of the renin-angiotensin-aldosterone system (RAAS) in response to low blood pressure.

• A. Angiotensinogen directly to angiotensin II with no intermediates.
• B. Juxtaglomerular cells release renin → angiotensinogen to angiotensin I → ACE converts to angiotensin II → vasoconstriction and aldosterone release → increased sodium and water retention → BP rises.
• C. Aldosterone acts to decrease sodium retention.
• D. ACE inhibits renin release.

Answer: (B)

When blood pressure is low, the body activates the renin-angiotensin-aldosterone system to raise it. Juxtaglomerular cells in the kidney release renin, which cleaves angiotensinogen (made in the liver) to form angiotensin I. Angiotensin-converting enzyme, mainly in the lungs, converts angiotensin I to angiotensin II. Angiotensin II is a strong vasoconstrictor and also signals the adrenal cortex to release aldosterone. Aldosterone promotes sodium (and thus water) reabsorption in the distal nephron, increasing blood volume and raising blood pressure. Angiotensin II can also promote thirst and ADH release to help restore pressure. As blood pressure rises, renin release is reduced through negative feedback.

This sequence explains why the option describing renin release, formation of angiotensin II via angiotensin I, the vasoconstrictive effects, and aldosterone-driven sodium and water retention fits best.