In the renal context, ACE inhibitors play a key role in controlling intraglomerular pressure. By blocking angiotensin II formation, they reduce efferent arteriole constriction and help preserve filtration surface integrity. However, in patients with existing renal artery stenosis, ACE inhibitors can further reduce GFR — requiring cautious monitoring of serum creatinine and potassium levels.
Angiotensin-Converting Enzyme (ACE) inhibitors block the enzyme responsible for converting angiotensin I to angiotensin II, a powerful vasoconstrictor. By reducing angiotensin II levels, these drugs promote vasodilation, decrease sodium and water retention, and lower systemic vascular resistance. This action also decreases aldosterone secretion, which in turn reduces blood volume and preload.
In the renal context, ACE inhibitors play a key role in controlling intraglomerular pressure. By blocking angiotensin II formation, they reduce efferent arteriole constriction and help preserve filtration surface integrity. However, in patients with existing renal artery stenosis, ACE inhibitors can further reduce GFR — requiring cautious monitoring of serum creatinine and potassium levels.
From a hypertension standpoint, ACE inhibitors lower systemic vascular resistance by preventing angiotensin II–mediated vasoconstriction. They are often prescribed early in therapy, particularly for younger, non-Black patients or those with comorbid heart failure or diabetes. Emphasize patient adherence, monitoring of orthostatic changes, and the importance of avoiding potassium-rich salt substitutes.
In diabetic nephropathy, ACE inhibitors are essential in slowing disease progression. They reduce glomerular capillary hypertension and proteinuria by relaxing efferent arterioles. Regular monitoring of kidney function and microalbumin levels is essential. Educate patients about consistent medication use and reporting signs of dizziness, weakness, or swelling.