Our group has studied the morphological influences of Renin-Angiotensin-Aldosterone System (RAAS) inhibitors on the renal afferent arterioles. Studies were performed using Angiotensin II type1 Receptor Blockers (ARBs), an Angiotensin Converting Enzyme inhibitor (ACEi), and a Direct Renin Inhibitor (DRI) with several strains of rats. The same results were found in these experiments except DRI. The long-term administration of ARBs or ACEi both induced unusual severe proliferative changes of the renal afferent arteriolar walls and narrowed the lumens. The smooth muscle cells (SMCs) of the proliferative arteriolar walls were considered to be de-differentiated SMCs, which were originally renin cells. The renin granules were evidently increased in the juxtaglomerular apparatus cells by all the RAAS inhibitors. The increased renin granules were also found in the outer layers of SMCs in the treatment of ARBs/ACEi, and sometimes extended from the entrance of the glomeruli to the bifurcation of the interlobular arteries. Our group found the same results in humans by the treatment of ARB and/or ACEi.
The RAAS inhibitors are widely known to have the potential to influence the intra-glomerular hemodynamics and the organ-protective effects in essential hypertension or secondary hypertension. However, the long-term administration of ARB and/or ACEi include the ability to affect the afferent arteriolar walls in the kidney. It is necessary to give serious attention to the influences and the results of the blockade of the RAAS cascade in the kidney. Further studies on the beneficial methods of using these agents for the kidney are needed.
Angiotensin II type1 receptor blocker, RAAS inhibitors, Renal afferent arteriole, Morphology