Enhanced nitric oxide generation in root transition zone during the early stage of cadmium stress is required for maintaining root growth in barley

2015 ◽  
Vol 390 (1-2) ◽  
pp. 213-222 ◽  
Author(s):  
Aster Alemayehu ◽  
Veronika Zelinová ◽  
Beáta Bočová ◽  
Jana Huttová ◽  
Igor Mistrík ◽  
...  
2007 ◽  
Vol 293 (2) ◽  
pp. R707-R713 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Barbara K. Kemp-Harper ◽  
Helena C. Parkington ◽  
Geoffrey A. Head ◽  
Roger G. Evans

We determined whether nitric oxide (NO) counters the development of hypertension at the onset of diabetes in mice, whether this is dependent on endothelial NO synthase (eNOS), and whether non-NO endothelium-dependent vasodilator mechanisms are altered in diabetes in mice. Male mice were instrumented for chronic measurement of mean arterial pressure (MAP). In wild-type mice, MAP was greater after 5 wk of Nω-nitro-l-arginine methyl ester (l-NAME; 100 mg·kg−1·day−1 in drinking water; 97 ± 3 mmHg) than after vehicle treatment (88 ± 3 mmHg). MAP was also elevated in eNOS null mice (113 ± 4 mmHg). Seven days after streptozotocin treatment (200 mg/kg iv) MAP was further increased in l-NAME-treated mice (108 ± 5 mmHg) but not in vehicle-treated mice (88 ± 3 mmHg) nor eNOS null mice (104 ± 3 mmHg). In wild-type mice, maximal vasorelaxation of mesenteric arteries to acetylcholine was not altered by chronic l-NAME or induction of diabetes but was reduced by 42 ± 6% in l-NAME-treated diabetic mice. Furthermore, the relative roles of NO and endothelium-derived hyperpolarizing factor (EDHF) in acetylcholine-induced vasorelaxation were altered; the EDHF component was enhanced by l-NAME and blunted by diabetes. These data suggest that NO protects against the development of hypertension during early-stage diabetes in mice, even in the absence of eNOS. Furthermore, in mesenteric arteries, diabetes is associated with reduced EDHF function, with an apparent compensatory increase in NO function. Thus, prior inhibition of NOS results in endothelial dysfunction in early diabetes, since the diabetes-induced reduction in EDHF function cannot be compensated by increases in NO production.


2010 ◽  
Vol 173 (6) ◽  
pp. 885-891 ◽  
Author(s):  
Danielle Peres da Rocha Oliveiros Marciano ◽  
Flávia Toledo Ramos ◽  
Marina Neiva Alvim ◽  
Jose Ronaldo Magalhaes ◽  
Marcel Giovanni Costa França

2018 ◽  
Vol 37 (5) ◽  
pp. 1645-1653 ◽  
Author(s):  
Mariëlle P.K.J. Engelen ◽  
V. Suzanne Klimberg ◽  
Arianna Allasia ◽  
Nicolaas E.P. Deutz

2005 ◽  
Vol 288 (4) ◽  
pp. F694-F702 ◽  
Author(s):  
Ki-Hwan Han ◽  
Jung-Mi Lim ◽  
Wan-Young Kim ◽  
Hyang Kim ◽  
Kirsten M. Madsen ◽  
...  

Endothelium-derived nitric oxide (NO) is synthesized within the developing kidney and may play a crucial role in the regulation of renal hemodynamics. The purpose of this study was to establish the expression and intrarenal localization of the NO-synthesizing enzyme endothelial NO synthase (eNOS) during kidney development. Rat kidneys from 14 ( E14)-, 16 ( E16)-, 18 ( E18)-, and 20-day-old ( E20) fetuses and 1 ( P1)-, 3 ( P3)-, 7 ( P7)-, 14 ( P14)-, and 21-day-old ( P21) pups were processed for immunocytochemical and immunoblot analysis. In fetal kidneys, expression of eNOS was first observed in the endothelial cells of the undifferentiated intrarenal capillary network at E14. At E16, strong eNOS immunoreactivity was observed in the endothelial cells of renal vesicles, S-shaped bodies (stage II glomeruli), and stage III glomeruli at the corticomedullary junction. At E18- 20, early-stage developing glomeruli located in the subcapsular region showed less strong eNOS immunoreactivity than those of E16. The eNOS-positive immature glomeruli were observed in the nephrogenic zone until 7 days after birth. In fetal kidneys, eNOS was also expressed in the medulla in the endothelial cells of the capillaries surrounding medullary collecting ducts. After birth, eNOS immunostaining gradually increased in the developing vascular bundles and peritubular capillaries in the medulla and was highest at P21. Surprisingly, eNOS was also expressed in proximal tubules, in the endocytic vacuolar apparatus, only at P1. The strong expression of eNOS in the early stages of developing glomeruli and vasculature suggests that eNOS may play a role in regulating renal hemodynamics of the immature kidney.


PROTOPLASMA ◽  
2017 ◽  
Vol 255 (1) ◽  
pp. 79-93 ◽  
Author(s):  
Parvaiz Ahmad ◽  
Mohammed Abass Ahanger ◽  
Mohammed Nasser Alyemeni ◽  
Leonard Wijaya ◽  
Pravej Alam

Author(s):  
Celeste Molina‐Favero ◽  
Cecilia Mónica Creus ◽  
María Luciana Lanteri ◽  
Natalia Correa‐Aragunde ◽  
María Cristina Lombardo ◽  
...  

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