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

Role of Intrarenal Bradykinin

HIROTO MATSUDA^*, KOICHI HAYASHI^*, KOKI ARAKAWA^*, MAREO NAITOH^*, EIJI KUBOTA^*, MASANORI HONDA^*, AKIRA MATSUMOTO^*, HIROMICHI SUZUKI, TOKUNORI YAMAMOTO, FUMIHIKO KAJIYA and TAKAO SARUTA^*

^* Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
Department of Nephrology, Saitama Medical School, Saitama, Japan
Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Okayama, Japan.

Correspondence to Dr. Takao Saruta, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan. Phone: +81 3 3353 1211, extension 2312; Fax: +81 3 3359 2745; E-mail: saruta{at}mc.med.keio.ac.jp

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 (N-adamantaneacetyl-D-Arg-[Hyp³,Thi^5,8,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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