Nitric oxide synthase in macula densa regulates glomerular capillary pressure.

• DOI: 10.1073/pnas.89.24.11993
• Publication Date: 2006-05-31T12:14:57Z
• Authors: C S Wilcox; W J Welch; F Murad; S S Gross; G Taylor; R Levi; H H Schmidt
• Keywords: Macula densa; Tubuloglomerular feedback; Afferent arterioles; Tubular fluid; Loop of Henle

Tubular-fluid reabsorption by specialized cells of the nephron at junction ascending limb loop Henle and distal convoluted tubule, termed macula densa, releases compounds causing vasoconstriction adjacent afferent arteriole. Activation this tubuloglomerular feedback response reduces glomerular capillary pressure and, hence, filtration rate. The functions in a negative-feedback mode to relate tubular-fluid delivery reabsorption. This system has been implicated renal autoregulation, renin release, longterm body fluid blood-pressure homeostasis. Here we report that arginine-derived nitric oxide, generated is an additional intercellular signaling molecule released during counters Antibody rat cerebellar constitutive oxide synthase stained densa specifically. Microperfusion segment single nephrons with N omega-methyl-L-arginine (an inhibitor synthase) or pyocyanin (a lipid-soluble endothelium-derived relaxation factor) showed generation can vasodilate arteriole increase pressure; effect was blocked drugs prevent We conclude activated mediates vasodilating component response. These findings imply role for fluid-volume homeostasis, addition its established roles modulation vascular tone endothelium neurotransmission.