From the Research
Angiotensin Receptor Blockers (ARBs) primarily act on the efferent arteriole of the nephron, as well as having effects on the proximal tubule and collecting duct. The mechanism of action of ARBs involves selectively blocking the angiotensin II type 1 (AT1) receptors, which are abundantly present in the efferent arteriole 1. By blocking these receptors, ARBs prevent the vasoconstriction of the efferent arteriole that would normally occur in response to angiotensin II. This mechanism leads to dilation of the efferent arteriole, which reduces intraglomerular pressure and decreases glomerular filtration rate (GFR) 2. Some key points to consider when using ARBs include:
- They are highly effective antihypertensive agents that are also particularly well tolerated 2
- They can be used as first-line therapy or added at later stages of treatment titration 2
- They are very effective in combination with thiazide diuretics or calcium channel blockers 2 Additionally, ARBs have effects on the proximal tubule where they reduce sodium reabsorption, and on the collecting duct where they decrease water reabsorption by inhibiting the release of aldosterone 3, 4, 5. This comprehensive action throughout the nephron explains why ARBs are effective antihypertensive medications and provide renoprotective effects, particularly in patients with diabetic nephropathy or chronic kidney disease with proteinuria. It's worth noting that while there are some differences in the pharmacology of different ARBs, such as their affinity for the AT1 receptor and the mechanism by which they block the receptor, these differences do not appear to have a significant impact on their clinical efficacy 5.