scholarly journals Regulation of Annexin A1 in the macula densa: association with neuronal nitric oxide synthase and cyclooxygenase‐2

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Alexander Paliege ◽  
Saskia Seidel ◽  
Tom Roschel ◽  
Kerim Mutig ◽  
Sebastian Bachmann
2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Alexander Paliege ◽  
Thomas Kahl ◽  
Saskia Seidel ◽  
Jürgen Schnermann ◽  
Sebastian Bachmann

1998 ◽  
Vol 274 (3) ◽  
pp. F516-F524 ◽  
Author(s):  
Atsuhiro Ichihara ◽  
Edward W. Inscho ◽  
John D. Imig ◽  
L. Gabriel Navar

This study was performed to determine the influence of neuronal nitric oxide synthase (nNOS) on renal arteriolar tone under conditions of normal, interrupted, and increased volume delivery to the macula densa segment and on the microvascular responses to angiotensin II (ANG II). Experiments were performed in vitro on afferent (21.2 ± 0.2 μm) and efferent (18.5 ± 0.2 μm) arterioles of kidneys harvested from male Sprague-Dawley rats, using the blood-perfused juxtamedullary nephron technique. Superfusion with the specific nNOS inhibitor, S-methyl-l-thiocitrulline (l-SMTC), decreased afferent and efferent arteriolar diameters, and these decreases in arteriolar diameters were prevented by interruption of distal volume delivery by papillectomy. When 10 mM acetazolamide was added to the blood perfusate to increase volume delivery to the macula densa segment, afferent arteriolar vasoconstrictor responses tol-SMTC were enhanced, but this effect was again completely prevented after papillectomy. In contrast, the arteriolar diameter responses to the nonselective NOS inhibitor, N ω-nitro-l-arginine (l-NNA) were only attenuated by papillectomy.l-SMTC (10 μM) enhanced the efferent arteriolar vasoconstrictor response to ANG II but did not alter the afferent arteriolar vasoconstrictor responsiveness to ANG II. In contrast, l-NNA (100 μM) enhanced both afferent and efferent arteriolar vasoconstrictor responses to ANG II. These results indicate that the modulating influence of nNOS on afferent arteriolar tone of juxtamedullary nephrons is dependent on distal tubular fluid flow. Furthermore, nNOS exerts a differential modulatory action on the juxtamedullary microvasculature by enhancing efferent, but not afferent, arteriolar responsiveness to ANG II.


2004 ◽  
Vol 53 (4) ◽  
pp. 387-390 ◽  
Author(s):  
Akira YABUKI ◽  
Mitsuharu MATSUMOTO ◽  
Ryozo KAMIMURA ◽  
Kazuyuki TANIGUCHI ◽  
Syusaku SUZUKI

2009 ◽  
Vol 46 (3) ◽  
pp. 188-198 ◽  
Author(s):  
Nathalie Krattinger ◽  
Florian Alonso ◽  
Alessandro Capponi ◽  
Lucia Mazzolai ◽  
Pascal Nicod ◽  
...  

2006 ◽  
Vol 39 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Akihiro Tojo ◽  
Maristela Lika Onozato ◽  
Toshiro Fujita

2018 ◽  
Vol 314 (6) ◽  
pp. F1197-F1204 ◽  
Author(s):  
Sungmi Park ◽  
Benjamin J. Bivona ◽  
Lisa M. Harrison-Bernard

We have previously reported significant increases in neuronal nitric oxide synthase (NOS) immunostaining in renal arterioles of angiotensin type 1A receptor (AT1A) knockout mice, and in arterioles and macula densa cells of AT1A/AT1B knockout mice. The contribution of nitric oxide derived from endothelial and macula densa cells in the maintenance of afferent arteriolar tone and acetylcholine-induced vasodilation was functionally determined in kidneys of wild-type, AT1A, and AT1A/AT1B knockout mice. Acetylcholine-induced changes in arteriolar diameters of in vitro blood-perfused juxtamedullary nephrons were measured during control conditions, in the presence of the nonspecific NOS inhibitor, Nω-nitro-l-arginine methyl ester (NLA), or the highly selective neuronal NOS inhibitor, N5-(1-imino-3-butenyl)-l-ornithine (VNIO). Acetylcholine (0.1 mM) produced a significant vasoconstriction in afferent arterioles of AT1A/AT1B mice (−10.9 ± 5.1%) and no changes in afferent arteriolar diameters of AT1A knockout mice. NLA (0.01–1 mM) or VNIO (0.01–1 μM) induced significant dose-dependent vasoconstrictions (−19.8 ± 4.0% 1 mM NLA; −7.8 ± 3.5% 1 μM VNIO) in afferent arterioles of kidneys of wild-type mice. VNIO had no effect on afferent arteriole diameters of AT1A knockout or AT1A/AT1B knockout mice, suggesting nonfunctional neuronal nitric oxide synthase. These data indicate that acetylcholine produces a significant renal afferent arteriole vasodilation independently of nitric oxide synthases in wild-type mice. AT1A receptors are essential for the manifestation of renal afferent arteriole responses to neuronal nitric oxide synthase-mediated nitric oxide release.


2000 ◽  
Vol 441 (2-3) ◽  
pp. 235-240 ◽  
Author(s):  
Hayo Castrop ◽  
Martin Kammerl ◽  
Bianca Mann ◽  
Boye L. Jensen ◽  
Bernhard K. Krämer ◽  
...  

2001 ◽  
Vol 60 (5) ◽  
pp. 1676-1683 ◽  
Author(s):  
Yilin Ren ◽  
Jeffrey L. Garvin ◽  
Sadayoshi Ito ◽  
Oscar A. Carretero

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