Endothelial permeability of the afferent arteriole and its changes as the result of alteration in the activity of the renin-angiotensin system.
Recent studies have demonstrated fenestrations in the juxtaglomerular part of the afferent arteriole facing the extraglomerular mesangium and the epithelioid cells in different mammals including humans. The permeability of the endothelium in afferent arteriole may play an important role in various physiologic and pathophysiologic processes. This study therefore was conducted to examine the permeability along the length of afferent arteriole using ferritin particles as an indicator of permeability/fenestration. Assuming the presence of a relationship between the development of permeable endothelial fenestration and renin formation, the permeability of the endothelium and renin granulation and their correlation along the wall of the afferent arteriole under control conditions and during inhibition of renin-angiotensin system by converting enzyme inhibition or AT1 receptor blockade were examined. The intra-aortically administered ferritin particles appeared in the interstitium of the distal part of the afferent arterioles. About one-third to half of the length of the afferent arteriole wall was ferritin-positive. There was a correlation between ferritin-positive and renin-positive portions. The density of ferritin particles was high close to the glomerulus and decreased continuously, similar to the profile of renin distribution. There was also a correlation between ferritin density in basal membrane and the renin granulation index. On the basis of these results, the afferent arteriole, according to its endothelial permeability, can be divided into two distinct portions, i.e., the permeable and the nonpermeable, the length and ratio of which may be related to the actual renin formation. These portions not only are different in the presence or absence of fenestration of the endothelium, but they also show difference in myosin and renin contents, suggesting that each portion may serve different function(s).
Rosivall
L
L
Department of Pathophysiology, International Nephrology Research and Training Center, Semmelweis University of Medicine, Budapest, Hungary. roslasz@net.sote.hu
Rázga
Z
Z
Mirzahosseini
S
S
Tornóci
L
L
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005293:Ferritins / Q000032:analysis / Q000494:pharmacology; D009218:Myosins / Q000032:analysis; D010539:Permeability; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D012083:Renin / Q000032:analysis; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D013777:Tetrazoles
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D013777:Tetrazoles; D005293:Ferritins; D002216:Captopril; D012083:Renin; D009218:Myosins; C077793:candesartan cilexetil