Effect of nadph oxidase inhibitor and superoxide dismutase mimetic on the expression of nitric oxide synthase in spontaneously hypertensive rats

2009 ◽  
Vol 137 ◽  
pp. S144
Author(s):  
P. CAO ◽  
O. ITO ◽  
Q. GUO ◽  
D. ITO ◽  
Y. MUROYA ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Nadph Oxidase ◽  
Spontaneously Hypertensive Rats ◽  
Oxidase Inhibitor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nadph Oxidase Inhibitor ◽  
Oxide Synthase

Superoxide Dismutase Mimetic Increases Neuronal Nitric Oxide Synthase Influence on Afferent Arteriolar Diameter in Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 712-713
Author(s):  
Atsuhiro Ichihara ◽  
Matsuhiko Hayashi ◽  
Nobuhisa Hirota ◽  
Takao Saruta
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Superoxide Anion ◽  
Spontaneously Hypertensive Rats ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Arteriolar Diameter

P108 This study was designed to determine the influence of increased superoxide anion production in neuronal nitric oxide synthase (nNOS)-dependent regulation of afferent arteriolar diameter in spontaneously hypertensive rats (SHR). Afferent arteriolar diameters of male Wister-Kyoto rats (WKY) and SHR (300-350 g) were assessed in vitro using the blood-perfused juxtamedullary nephron technique and averaged 21.6 ± 1.6 (n = 6) and 18.8 ± 1.2 μm (n = 7); respectively. Superfusion with the superoxide dismutase mimetic, tempol (1, 10, and 100 μmol/L), did not influence afferent arteriolar diameters of WKY, but significantly increased afferent arteriolar diameters of SHR by 20.6 ± 5.5%, 25.2 ± 5.4% and 23.3 ± 4.9%; respectively. In WKY (n = 6), superfusion with the nNOS inhibitor, S -methyl-L-thiocitrulline (L-SMTC; 10 μmol/L), and the NOS inhibitor, N w -nitro-L-arginine (L-NNA; 100 μmol/L), significantly decreased afferent arteriolar diameters (19.6 ± 1.6 μm) by 11.9 ± 3.1% and 21.0 ± 3.9%; respectively. In SHR (n = 7), L-SMTC treatment did not influence afferent arteriolar diameters (21.0 ± 1.5 μm), but L-NNA treatment exerted a significant afferent arteriolar constriction (14.8 ± 3.2%) which was similar to that observed in WKY. Experiments were also performed in the presence of 100 μmol/L tempol. In WKY (n = 6), tempol treatment did not modulate basal afferent arteriolar diameters (21.5 ± 1.2 μm) or afferent arteriolar constrictor responses to L-SMTC (10.6 ± 2.1%) and L-NNA (19.3 ± 3.3%). In SHR (n = 8), tempol treatment significantly increased afferent arteriolar diameters by 22.5 ± 4.3% and enhanced afferent arteriolar constrictor responses to L-SMTC (18.4 ± 2.7%) and L-NNA (31.9 ± 2.6%). However, superfusion with the nitric oxide donor, S -nitroso-N-acetylpenicillamine (10 μmol/L), which exerted a similar afferent arteriolar vasodilation (19.7 ± 3.8%, n = 4), did not influence afferent arteriolar responses to L-SMTC (-2.1 ± 3.1%) or L-NNA (15.1 ± 3.3%). These results suggest that increased superoxide anion inhibits nNOS-dependent regulation of afferent arteriolar diameters in SHR.

Expression of endothelin receptors and nitric oxide synthase in the brain of stroke-prone spontaneously hypertensive rats with cerebral apoplexy

1997 ◽  
Vol 756 (1-2) ◽  
pp. 61-67 ◽  
Author(s):  
Yasuko Sakurai-Yamashita ◽  
Kimihiro Yamashita ◽  
Yasufumi Kataoka ◽  
Akihiko Himeno ◽  
Masami Niwa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Endothelin Receptors ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
The Brain

scholarly journals Rapamycin Induces an eNOS (Endothelial Nitric Oxide Synthase) Dependent Increase in Brain Collateral Perfusion in Wistar and Spontaneously Hypertensive Rats

Stroke ◽  
2020 ◽  
Vol 51 (9) ◽  
pp. 2834-2843
Author(s):  
Daniel J. Beard ◽  
Zhaojin Li ◽  
Anna M. Schneider ◽  
Yvonne Couch ◽  
Marilyn J. Cipolla ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Infarct Volume ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background and Purpose: Rapamycin is a clinically approved mammalian target of rapamycin inhibitor that has been shown to be neuroprotective in animal models of stroke. However, the mechanism of rapamycin-induced neuroprotection is still being explored. Our aims were to determine if rapamycin improved leptomeningeal collateral perfusion, to determine if this is through eNOS (endothelial nitric oxide synthase)-mediated vessel dilation and to determine if rapamycin increases immediate postreperfusion blood flow. Methods: Wistar and spontaneously hypertensive rats (≈14 weeks old, n=22 and n=15, respectively) were subjected to ischemia by middle cerebral artery occlusion (90 and 120 minutes, respectively) with or without treatment with rapamycin at 30-minute poststroke. Changes in middle cerebral artery and collateral perfusion territories were measured by dual-site laser Doppler. Reactivity to rapamycin was studied using isolated and pressurized leptomeningeal anastomoses. Brain injury was measured histologically or with triphenyltetrazolium chloride staining. Results: In Wistar rats, rapamycin increased collateral perfusion (43±17%), increased reperfusion cerebral blood flow (16±8%) and significantly reduced infarct volume (35±6 versus 63±8 mm 3 , P <0.05). Rapamycin dilated leptomeningeal anastomoses by 80±9%, which was abolished by nitric oxide synthase inhibition. In spontaneously hypertensive rats, rapamycin increased collateral perfusion by 32±25%, reperfusion cerebral blood flow by 44±16%, without reducing acute infarct volume 2 hours postreperfusion. Reperfusion cerebral blood flow was a stronger predictor of brain damage than collateral perfusion in both Wistar and spontaneously hypertensive rats. Conclusions: Rapamycin increased collateral perfusion and reperfusion cerebral blood flow in both Wistar and comorbid spontaneously hypertensive rats that appeared to be mediated by enhancing eNOS activation. These findings suggest that rapamycin may be an effective acute therapy for increasing collateral flow and as an adjunct therapy to thrombolysis or thrombectomy to improve reperfusion blood flow.

Effect of apocynin treatment on renal expression of COX-2, NOS1, and renin in Wistar-Kyoto and spontaneously hypertensive rats

2006 ◽  
Vol 290 (3) ◽  
pp. R694-R700 ◽  
Author(s):  
A. Paliege ◽  
A. Parsumathy ◽  
D. Mizel ◽  
T. Yang ◽  
J. Schnermann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Oxidase Inhibitor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cox 2 ◽  
Wistar Kyoto

Macula densa (MD) cells of the juxtaglomerular apparatus (JGA) synthesize type 1 nitric oxide synthase (NOS1) and type 2 cyclooxygenase (COX-2). Both nitric oxide (NO) and prostaglandins have been considered to mediate or modulate the control of renin secretion. Reactive oxygen species (ROS) produced locally by NADPH oxidase may influence NO bioavailability. We have tested the hypothesis that in hypertension elevated ROS levels may modify the expression of NOS1 and COX-2 in the JGA, thereby interacting with juxtaglomerular signaling. To this end, spontaneously hypertensive rats (SHR) and Wistar-Kyoto control rats (WKY) received the specific NADPH oxidase inhibitor, apocynin, during 3 wk. Renal functional and histochemical parameters, plasma renin activity (PRA), and as a measure of ROS activity, urinary isoprostane excretion (IP) were evaluated. Compared with WKY, IP levels in untreated SHR were 2.2-fold increased, and NOS1 immunoreactiviy (IR) of JGA 1.5-fold increased, whereas COX-2 IR was reduced to 35%, renin IR to 51%, and PRA to 7%. Apocynin treatment reduced IP levels in SHR to 52%, NOS1 IR to 69%, and renin IR to 62% of untreated SHR, whereas renin mRNA, COX-2 IR, glomerular filtration rate, PRA, and systolic blood pressure remained unchanged. WKY revealed no changes under apocynin treatment. These data show that NADPH oxidase is an important contributor to elevated levels of ROS in hypertension. Upregulation of MD NOS1 in SHR may have the potential of blunting the functional impact of ROS at the level of bioavailable NO. Downregulated COX-2 and renin levels in SHR are apparently unrelated to oxidative stress, since apocynin treatment had no effect on these parameters.

Sign in / Sign up

Export Citation Format

Share Document