This has led to some bias in the evidence base underpinning recommendations for using ACE-Is or ARBs in the treatment of BP. There is no substantive evidence to suggest that ACE-Is and ARBs differ in their ability to reduce BP in patients with In most health care settings, ACE-Is are less expensive than ARBs, which may influence the choice between an ACE-I or ARB. The most prominent BP-related effects of the blockade of angiotensin II by ACE-Is or ARBs are as follows: K Generalized arterial vasodilatation, resulting in lower BP. K Vasodilatation of the efferent and afferent glomerular arterioles, particularly the efferent, resulting in decreased intra-glomerular pressure and hence reduction in both GFR and urine albumin excretion. This is believed to result in some degree of long-term renoprotection, at least in patients with albuminuria.87 On initiation of therapy a reversible reduction in GFR of up to 30% (accordingly a 30% increase in SCr concentration) has been regarded as reasonably attributable to this physio- logical mechanism. Greater reductions may indicate underlying renal artery stenosis.1,88 It has been suggested that in advanced CKD, cessation of RAAS blockade may allow an increase in GFR of sufficient magnitude to delay end-stage kidney failure.23 This concept is further discussed in Chapter 8. K Reduction in adrenal secretion of aldosterone. In about 50% of subjects prescribed ACE-Is or ARBs, aldosterone production is restored to at least pre-treatment levels over a period of months (a phenomenon termed aldosterone This may explain the efficacy of aldosterone antagonists in patients already taking an ACE-I or ARB. ACE-Is and ARBs may have other effects, including inhibition of fibrosis and enhancement of vascular and cardiac remodelling. Discussion of these effects, which may be of relevance to renoprotection, is beyond the scope of this Guideline. Dose considerations in CKD patients. 