The knowledge and the information about Renin Angiotensin System and Arginine-Nitric Oxide pathway helped us in understanding more about cardiac, vascular and renal systems, their function, the physiology, and pathophysiology of different diseases that may affect them. The existence of a Nitric Oxide/Angiotensin II axis, brought modification to our ways of thinking with new and more pathophysiological approaches to the treatment of hypertension and end-organ disease. There appears to be a link between hypertension, salt sensitivity, endothelial function and NO-AnglI axis on one side and end organ damage on the other side. Anti-hypertensive agents that can restore endothelial function beside their antihypertensive effect, may be better in preventing or at least slowing end-organ damage.

Angiotensin II↗

PubMedDate not supplied

Role of hypertension in progressive glomerular immune injury.

The relationship between hypertension, ferritin-antiferritin mesangial immune injury (FIC), and progressive glomerular damage was studied in hypertensive (8% NaCl chow) Dahl salt-sensitive rats (DS) and in spontaneously hypertensive rats (SHR). The glomeruli of SHR are protected from the increased perfusion pressure that accompanies systemic hypertension by preglomerular vasoconstriction, while the glomeruli of hypertensive DS are not. Blood pressure, serum creatinine levels, urinary protein excretion, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined in 20-week-old SHR and DS with FIC. In addition, half of a group of 20-week-old SHR with FIC were uninephrectomized and progression of glomerular injury was assessed 12 weeks later. Control rats for each of the groups did not receive FIC. Our studies showed that more extensive mesangial expansion and glomerulosclerosis developed in hypertensive DS with FIC than in rats without FIC. Glomerular injury in DS with FIC affected cortical and deep glomeruli. Similarly, hypertensive SHR with FIC had minimal damage in cortical glomeruli. In deep glomeruli of SHR, mesangial expansion was similar to that of DS, but glomerulosclerosis was absent. In SHR, a 50% reduction in renal mass, a maneuver known to decrease preglomerular vasoconstriction, resulted in mesangial expansion similar to that in DS in cortical glomeruli while deep glomeruli developed mesangial expansion as well as glomerulosclerosis. Our results suggest that when hypertension and mesangial immune injury coexist with renal vasodilatation (as occurs in DS with 2 kidneys and in SHR after uninephrectomy), they act synergistically to induce progressive glomerular damage. Similar mechanisms may be operative in hypertensive humans with glomerulonephritis and may condition the rate of progression to renal insufficiency.

Animals↗