scholarly journals Functional and Biochemical Endothelial Profiling In Vivo in a Murine Model of Endothelial Dysfunction; Comparison of Effects of 1-Methylnicotinamide and Angiotensin-converting Enzyme Inhibitor

2017 ◽  
Vol 8 ◽  
Author(s):  
Anna Bar ◽  
Mariola Olkowicz ◽  
Urszula Tyrankiewicz ◽  
Edyta Kus ◽  
Krzysztof Jasinski ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Murine Model ◽  
Enzyme Inhibitor ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor

scholarly journals Zonal Heterogeneity in Action of Angiotensin-Converting Enzyme Inhibitor on Renal Microcirculation

1999 ◽  
Vol 10 (11) ◽  
pp. 2272-2282
Author(s):  
HIROTO MATSUDA ◽  
KOICHI HAYASHI ◽  
KOKI ARAKAWA ◽  
MAREO NAITOH ◽  
EIJI KUBOTA ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Sodium Excretion ◽  
Enzyme Inhibitor ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Bradykinin Antagonist ◽  
Glomerular Hemodynamics ◽  
Nitrite Nitrate

Abstract. The present study examined the role of intrarenal bradykinin in angiotensin-converting enzyme inhibitor (ACEI)-induced dilation of renal afferent (AFF) and efferent arterioles (EFF) in vivo, and further evaluated whether ACEI-stimulated bradykinin activity differed in superficial (SP) and juxtamedullary nephrons (JM). Arterioles of canine kidneys were visualized with an intravital charge-coupled device camera microscope. E4177 (an angiotensin receptor antagonist, 30 μg/kg) dilated AFF and EFF in SP (15 ± 3% and 19 ± 5%) and JM (15 ± 3% and 18 ± 4%). Subsequently, cilazaprilat (30 μg/kg) caused further dilation of both AFF (29 ± 4%) and EFF (36 ± 4%) in JM, whereas in SP it dilated only EFF (29 ± 3%). Similarly, in the presence of E4177, cilazaprilat caused further increases in sodium excretion. This cilazaprilat-induced vasodilation and natriuresis was abolished by a bradykinin antagonist (Nα-adamantaneacetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-bradykinin). In parallel with these results, cilazaprilat increased renal bradykinin content, more greatly in the medulla than in the cortex (5.7 ± 0.4 versus 4.6 ± 0.1 ng/g). Similarly, cilazaprilat elicited greater bradykinin-dependent increases of nitrite/nitrate in the medulla. In conclusion, zonal heterogeneity in renal bradykinin/nitric oxide levels and segmental differences in reactivity to bradykinin contribute to the diverse responsiveness of renal AFF and EFF to ACEI. ACEI-enhanced kinin action would participate in the amelioration of glomerular hemodynamics and renal sodium excretion by ACEI.

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