Arrange the series of reactions that occurs when plasma volume and osmolarity are disturbed.

Arrange the series of reactions that occurs when plasma volume and osmolarity are disturbed.

• A. Change in posture -> Conversion of angiotensinogen to angiotensin I -> Formation of active form of angiotensin -> Increased reabsorption of water and sodium -> Increased blood volume
• B. Change in posture -> Formation of active form of angiotensin -> Conversion of angiotensinogen to angiotensin I -> Increased reabsorption of water and sodium -> Increased blood volume
• C. Increased blood volume -> Change in posture -> Conversion of angiotensinogen to angiotensin I -> Increased reabsorption of water and sodium -> Formation of active form of angiotensin
• D. Conversion of angiotensinogen to angiotensin I -> Change in posture -> Formation of active form of angiotensin -> Increased reabsorption of water and sodium -> Increased blood volume

Answer: (A)

Disturbances in plasma volume or osmolarity trigger the kidneys to activate the renin-angiotensin-aldosterone system to restore circulating volume. A change in posture can reduce venous return and renal perfusion, prompting the juxtaglomerular cells to release renin. Renin then cleaves angiotensinogen to angiotensin I. Angiotensin-converting enzyme converts angiotensin I to the active hormone angiotensin II. Angiotensin II promotes increased Na+ and water reabsorption and stimulates aldosterone release, leading to increased blood volume. This sequence—posture change initiating renin release, formation of angiotensin I, formation of the active angiotensin II, then enhanced reabsorption and volume expansion—best fits the process. Other sequences misplace these steps, such as presenting the active form before angiotensin I or implying blood volume rises before the RAAS is engaged.

Disturbances in plasma volume or osmolarity trigger the kidneys to activate the renin-angiotensin-aldosterone system to restore circulating volume. A change in posture can reduce venous return and renal perfusion, prompting the juxtaglomerular cells to release renin. Renin then cleaves angiotensinogen to angiotensin I. Angiotensin-converting enzyme converts angiotensin I to the active hormone angiotensin II. Angiotensin II promotes increased Na+ and water reabsorption and stimulates aldosterone release, leading to increased blood volume. This sequence—posture change initiating renin release, formation of angiotensin I, formation of the active angiotensin II, then enhanced reabsorption and volume expansion—best fits the process. Other sequences misplace these steps, such as presenting the active form before angiotensin I or implying blood volume rises before the RAAS is engaged.