Regarding the physiological actions of angiotensin II, all of the following are true EXCEPT:

## Angiotensin II: Mechanisms of Action **Key Point:** Angiotensin II is a potent vasoconstrictor that acts on AT1 and AT2 receptors to regulate blood pressure, fluid balance, and electrolyte homeostasis. ### Vascular Effects of Angiotensin II Angiotensin II causes **constriction of both afferent AND efferent arterioles**, but the effect on the efferent arteriole is MORE PRONOUNCED. This preferential constriction of the efferent arteriole: - Maintains glomerular filtration pressure despite systemic hypotension - Preserves GFR when renal perfusion pressure is low - Is a key compensatory mechanism in volume depletion **Warning:** A common misconception is that Ang II dilates the efferent arteriole — this is FALSE. Both vessels constrict, but efferent constriction dominates. ### Renal Tubular Effects | Effect | Mechanism | Result | |--------|-----------|--------| | Proximal tubule | Direct stimulation of Na-H exchanger (NHE3) | Increased Na+ reabsorption | | Collecting duct | Stimulates aldosterone secretion | Enhanced Na+ reabsorption, K+ excretion | | Thick ascending limb | Enhances Na-K-2Cl cotransport | Increased Na+ reabsorption | ### Aldosterone Stimulation Angiotensin II is the **primary physiological stimulus** for aldosterone release from the zona glomerulosa, independent of ACTH. **High-Yield:** The efferent arteriole constriction by Ang II is the reason ACE inhibitors and ARBs can cause acute kidney injury in patients with severe renal artery stenosis — loss of efferent constriction drops GFR precipitously. ### Why Option 3 Is Correct (The Exception) Angiotensin II **CONSTRICTS the efferent arteriole**, not dilates it. This constriction: - Increases glomerular capillary hydrostatic pressure - Maintains or increases GFR (not decreases it) - Opposes the effect of afferent constriction The statement that Ang II "decreases GFR by preferentially dilating the efferent arteriole" is mechanistically backward and contradicts established renal physiology. [cite:Guyton & Hall Textbook of Medical Physiology Ch 26]