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Nitric oxide generated by nNOS in the macula densa regulates the afferent arteriolar diameter in rat kidney

Authors
  • Tojo, Akihiro1
  • Onozato, Maristela Lika1
  • Fukuda, Satoru2
  • Asaba, Kensuke1
  • Kimura, Kenjiro1
  • Fujita, Toshiro1
  • 1 University of Tokyo, Division of Nephrology and Endocrinology, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan , Tokyo
  • 2 University of Tokyo, Laboratory of Electron Microscopy, Tokyo, Japan , Tokyo
Type
Published Article
Journal
Medical Electron Microscopy
Publisher
Springer-Verlag
Publication Date
Dec 01, 2004
Volume
37
Issue
4
Pages
236–241
Identifiers
DOI: 10.1007/s00795-004-0263-2
Source
Springer Nature
Keywords
License
Yellow

Abstract

Nitric oxide (NO) derived from neuronal NO synthase (nNOS) in the macula densa is a modulator of tubuloglomerular feedback. However, little is known about the regulation of the afferent arteriolar diameter by NO from the macula densa in salt-sensitive hypertension. We investigated the relationship between nNOS in the macula densa and the afferent arteriolar diameter in deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with angiotensin converting enzyme (ACE) inhibitor or thiazide for 5 weeks. DOCA rats had reduced nNOS expression in the macula densa compared to controls and reduction of NO production evaluated with 4,5-diaminofluorescein diacetate in the juxtaglomerular apparatus (JGA). Treatment with ACE inhibitor and thiazide increased nNOS and NO production in the JGA. The diameter of the afferent arteriole observed by SEM using microvascular casts was smaller in DOCA rats compared to control rats, and ACE inhibitor or thiazide dilated the afferent arteriole with a positive correlation to nNOS immunoreactivity in the macula densa. In conclusion, the afferent arteriolar diameter might be regulated by NO derived from nNOS in the macula densa in DOCA-salt hypertensive rats.

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