The Proliferative Changes of Renal Afferent Arteriolar Walls and Renin-Angiotensin-Aldosterone System Inhibitors

Abstract

The hyperfiltration theory of Brenner et al. in 1982 [1], is widely recognized and studied closely as a final common pathway of kidney function deterioration from some point to the irreversible end-stage by any first kidney insult. In the paper, the deterioration of kidney function is induced because of the glomerular hemodynamics, glomerular hyperfiltration, and glomerular hypertension. These are caused by the overload of remaining glomeruli from any kidney insult that is associated with the decrease in the number of glomeruli [2][3][4]. In glomeruli, the increase of blood flow in each glomerulus occurs when afferent arterioles dilate, such as diabetes [5,6] or obesity [7], and occurs when blood flow is relatively higher in the afferent than in the efferent arterioles. The glomerular blood flow and transglomerular pressure are regulated by afferent and efferent arteriolar constriction or dilation. The blood flow fluctuates in order to preserve intraglomerular pressure from the renal interlobular, arcuate, interlobar arteries, and through the renal arteries directly reflected by central blood pressure [8].Arterial and arteriolar constriction are known to be induced by vaso-constrictive substances, especially the strong vasoconstrictor angiotensin II, through the stimulation of the angiotensin II receptor type 1 in vessels. Then, after the publishing of the glomerular hyperfiltration theory, the role of activation in the renal Renin-Angiotensin-Aldosterone system (RAAS) was remarkably focused on the progression to the end-stage renal disease (ESRD) [3][4][5].Essential hypertension is known to be induced by the morphologic changes of vessels in many organs, especially intrarenal arteries and arterioles. The morphological changes of the interlobular arteries and the bigger size intrarenal arteries (arcuate, interlobar, renal artery, and its branches)