Re: Role of endothelin receptors and relationship with nitric oxide synthase in impaired erectile response in diabetic rats. Alkan E, Ugan RA, Basar MM, Halici Z, Karakus E, Balbay MD, Un H.Andrologia. 2016 May 4. doi: 10.1111/and.12607

Andrologia ◽  
2018 ◽  
Vol 50 (4) ◽  
pp. e13001
Author(s):  
E. Ozbek
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Endothelin Receptors ◽  
Erectile Response ◽  
Oxide Synthase

Role of endothelin receptors and relationship with nitric oxide synthase in impaired erectile response in diabetic rats

Andrologia ◽  
2016 ◽  
Vol 49 (2) ◽  
pp. e12607 ◽  
Author(s):  
E. Alkan ◽  
R. A. Ugan ◽  
M. M. Basar ◽  
Z. Halici ◽  
E. Karakus ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Endothelin Receptors ◽  
Erectile Response ◽  
Oxide Synthase

Role of neuronal nitric oxide synthase (NOS1) in the pathogenesis of renal hemodynamic changes in diabetes

2000 ◽  
Vol 279 (3) ◽  
pp. F573-F583 ◽  
Author(s):  
Radko Komers ◽  
Jessie N. Lindsley ◽  
Terry T. Oyama ◽  
Kristen M. Allison ◽  
Sharon Anderson
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Renal Plasma Flow ◽  
Diabetic Rats ◽  
Hemodynamic Changes ◽  
Renal Hemodynamic ◽  
Streptozotocin Diabetic Rats ◽  
Oxide Synthase ◽  
Nos Isoforms

Nitric oxide (NO) has been implicated in the pathogenesis of renal hemodynamic changes in diabetes mellitus. However, the contribution of nitric oxide synthase (NOS) isoforms to intrarenal production of NO in diabetes remains unknown. To explore the role of NOS1 in the control of renal hemodynamics in diabetes, we assessed renal responses to inhibition of NOS1 with S-methyl-l-thiocitrulline (SMTC; administered into the abdominal aorta) in moderately hyperglycemic streptozotocin-diabetic rats (D) and their nondiabetic (C) and normoglycemic diabetic counterparts. The contribution of other NOS isoforms was also evaluated by assessing the responses to nonspecific NOS inhibition [ N G-nitro-l-arginine methyl ester (l-NAME)] in SMTC-treated diabetic rats. The number of NOS1-positive cells in macula densa of D and C kidneys was also evaluated by immunohistochemistry. D rats demonstrated elevated glomerular filtration rate (GFR) compared with C. SMTC (0.05 mg/kg) normalized GFR in D but had no effect in C. SMTC-induced reduction of renal plasma flow (RPF) was similar in C and D. Normoglycemic diabetic rats demonstrated blunted renal hemodynamic responses to NOS1 inhibition compared with hyperglycemic animals. Mean arterial pressure was stable in all groups. l-NAME induced a further decrease in RPF, but not in GFR, in D rats treated with SMTC. Immunohistochemistry revealed increased numbers of NOS1-positive cells in D. These observations suggest that NOS1-derived NO plays a major role in the pathogenesis of renal hemodynamic changes early in the course of diabetes. NOS1 appears to be the most important isoform in the generation of hemodynamically active NO in this condition.

scholarly journals Role of inducible nitric oxide synthase in induction of RhoA expression in hearts from diabetic rats

2008 ◽  
Vol 79 (2) ◽  
pp. 322-330 ◽  
Author(s):  
Hesham Soliman ◽  
Graham P. Craig ◽  
Prabhakar Nagareddy ◽  
Violet G. Yuen ◽  
Guorong Lin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Vasculoprotective Role of Inducible Nitric Oxide Synthase at Inflammatory Coronary Lesions Induced by Chronic Treatment With Interleukin-1β in Pigs in Vivo

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Chronic Treatment ◽  
Interleukin 1Β ◽  
Coronary Lesions ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Neuronal nitric oxide synthase and systemic vasodilation in rats with cirrhosis

2000 ◽  
Vol 279 (6) ◽  
pp. F1110-F1115 ◽  
Author(s):  
Lieming Xu ◽  
Ethan P. Carter ◽  
Mamiko Ohara ◽  
Pierre-Yves Martin ◽  
Boris Rogachev ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Cirrhosis ◽  
Nitric Oxide Synthase ◽  
Control Treatment ◽  
Sodium Balance ◽  
Hyperdynamic Circulation ◽  
Molecular Approaches ◽  
Advanced Liver Cirrhosis ◽  
Oxide Synthase

Cirrhosis is typically associated with a hyperdynamic circulation consisting of low blood pressure, low systemic vascular resistance (SVR), and high cardiac output. We have recently reported that nonspecific inhibition of nitric oxide synthase (NOS) with nitro-l-arginine methyl ester reverses the hyperdynamic circulation in rats with advanced liver cirrhosis induced by carbon tetrachloride (CCl4). Although an important role for endothelial NOS (eNOS) is documented in cirrhosis, the role of neuronal NOS (nNOS) has not been investigated. The present study was carried out to specifically investigate the role of nNOS during liver cirrhosis. Specifically, physiological, biochemical, and molecular approaches were employed to evaluate the contribution of nNOS to the cirrhosis-related hyperdynamic circulation in CCl4-induced cirrhotic rats with ascites. Cirrhotic animals had a significant increase in water and sodium retention. In the aorta from cirrhotic animals, both nNOS protein expression and cGMP concentration were significantly elevated compared with control. Treatment of cirrhotic rats for 7 days with the specific nNOS inhibitor 7-nitroindazole (7-NI) normalized the low SVR and mean arterial pressure, elevated cardiac index, and reversed the positive sodium balance. Increased plasma arginine vasopressin concentrations in the cirrhotic animals were also repressed with 7-NI in association with diminished water retention. The circulatory changes were associated with a reduction in aortic nNOS expression and cGMP. However, 7-NI treatment did not restore renal function in cirrhotic rats (creatinine clearance: 0.76 ± 0.03 ml · min−1· 100 g body wt−1in cirrhotic rats vs. 0.79 ± 0.05 ml · min−1· 100 g body wt−1in cirrhotic rats+7-NI; P NS.). Taken together, these results indicate that nNOS-derived NO contributes to the development of the hyperdynamic circulation and fluid retention in cirrhosis.

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