COULD “RENOPROTECTIVE” PHARMACOLOGICAL AGENTS ACT VIA IMPROVED TISSUE OXYGENATION?
As outlined above, claims for the efficacy of ACE inhibitors argue that the reason that they have an advantage is that they reduce proteinuria. However, it is possible that these renoprotective agents act via other, as yet unidentified, mechanisms. We therefore asked whether ACE inhibitors could protect the kidney by improving interstitial oxygen delivery. Theoretically, they should be able to do this because they dilate the efferent arterioles, reduce renal vascular resistance and they should improve microvascular flow in the interstitium. To address this, we recently described an in vivo model in which the phosphorescence of an injected protoporphyrin is inversely related to microvascular pO2 (abstract; Norman et al, J Am Soc Nephrol 10:666A, 1999). This phosphorescence can be measured noninvasively on the surface of an exposed rat kidney. Preliminary findings suggest that an ACE inhibitor prevents the slow decline in pO2 within the kidney that occurs over a 3-hour period of observat
