Figure 1116

Soon after the release of this useful class of antihypertensive drugs, the syndrome of functional acute renal insufficiency was described as a class effect. This phenomenon was first observed in patients with renal artery stenosis, particularly when the entire renal mass was affected, as in bilateral renal artery stenosis or in renal transplants with stenosis to a solitary kidney [26]. Acute renal dysfunction appears to be related to loss of postglomerular efferent arteriolar vascular tone and in general is reversible after withdrawing the angiotensin-converting enzyme (ACE) inhibitor [27].

Inhibition of the ACE kinase II results in at least two important effects: depletion of angiotensin II and accumulation of bradykinin [28]. The role of the latter effect on renal perfusion pressure is not clear, A.

To understand the angiotensin I converting enzyme inhibitor-induced drop in glomerular filtration rate, it is important to understand the physiologic role of the renin-angiotensin system in the regulation of renal hemodynamics, B. When renal perfusion drops, renin is released into the plasma and lymph by the juxtaglomerular cells of the kidneys. Renin cleaves angiotensino-gen to form angiotensin I, which is cleaved further by converting enzyme to form angiotensin II, the principal effector molecule in this system. Angiotensin II participates in glomerular filtration rate regulation in a least two ways. First, angiotensin II increases arterial pressure—directly and acutely by causing vasoconstriction and more "chronically" by increasing body fluid volumes through stimulation of renal sodium retention; directly through an effect on the tubules, as well as by stimulating thirst

(Continued on next page)

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