Gender-related differences in advanced glycation endproducts, oxidative stress markers and nitric oxide synthases in rats

Wang, X.; Desai, Kaushik; Juurlink, Bernhard H.J.; Champlain, Jacques de; Wu, Lingyun

doi:10.1038/sj.ki.5000043

Cited by 55 publications

(34 citation statements)

References 39 publications

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“…Under normotensive conditions female rats have been shown to have greater renal NOS1 immunoreactivity and NOS3 protein expression (22,36,40,55). In hypertension, female rats have been shown to have greater NOS1 immunoreactivity (55) or no sex differences in NOS1 and NOS3 protein (12,22). While a majority of both the clinical and experimental data tends to support the hypothesis that NO levels are greater in females compared with males, the molecular mechanism responsible remains unclear.…”

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confidence: 75%

“…Whole body NO levels have been reported to be greater in females compared with males (13,16,29,36), and a sex difference in the NO pathway may contribute to sexual dimorphisms in cardiovascular and renal pathologies. Under normotensive conditions female rats have been shown to have greater renal NOS1 immunoreactivity and NOS3 protein expression (22,36,40,55). In hypertension, female rats have been shown to have greater NOS1 immunoreactivity (55) or no sex differences in NOS1 and NOS3 protein (12,22).…”

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confidence: 99%

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Renal NOS activity, expression, and localization in male and female spontaneously hypertensive rats

Sullivan

Pardieck

Hyndman

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Sullivan JC, Pardieck JL, Hyndman KA, Pollock JS. Renal NOS activity, expression, and localization in male and female spontaneously hypertensive rats. Am J Physiol Regul Integr Comp Physiol 298: R61-R69, 2010. First published November 4, 2009 doi:10.1152/ajpregu.00526.2009.-The goal of this study was to examine the status of the renal nitric oxide (NO) system by determining NO synthase (NOS) isoform activity and expression within the three regions of the kidney in 14-wk-old male and female spontaneously hypertensive rats (SHR). NOS activity, and NOS1 and NOS3 protein expressions and localization were comparable in the renal cortex and outer medulla of male and female SHR. In contrast, male SHR had significantly less NOS1 and NOS3 enzymatic activity (0 Ϯ 5 and 53 Ϯ 7 pmol ⅐ mg Ϫ1 ⅐ 30 min Ϫ1 , respectively) compared with female SHR (37 Ϯ 16 and 172 Ϯ 40 pmol ⅐ mg Ϫ1 ⅐ 30 min Ϫ1 , respectively). Lower levels of inner medullary NOS1 activity in male SHR were associated with less NOS1 protein expression [45 Ϯ 7 relative densitometric units (RDU)] and fewer NOS1-positive cells in the renal inner medulla compared with female SHR (79 Ϯ 12 RDU). Phosphorylation of NOS3 is an important determinant of NOS activity. Male SHR had significantly greater phosphorylation of NOS3 on threonine 495 in the renal cortex compared with females (0.25 Ϯ 0.05 vs. 0.15 Ϯ 0.06 RDU). NOS3 phosphorylation was comparable in males and females in the other regions of the kidney. cGMP levels were measured as an indirect index of NO production. cGMP levels were significantly lower in the renal cortex (0.08 Ϯ 0.01 pmol/mg) and inner medulla (0.43 Ϯ 0.02 pmol/mg) of male SHR compared with females (cortex: 0.14 Ϯ 0.02 pmol/mg; inner medulla: 0.56 Ϯ 0.02 pmol/mg). Our data suggest that the effect of the sex of the animal on NOS activity and expression is different in the three regions of the SHR kidney and supports the hypothesis that male SHR have lower NO bioavailability compared with females. nitric oxide synthase; kidney; sex; gender; cGMP NITRIC OXIDE (NO) is an important regulator of blood pressure and kidney function (3,15,43). Therefore, it is not surprising that NO deficiencies have been linked with hypertension and the progression of chronic renal disease in both patients and experimental animals (2, 3, 45). All three NO synthase (NOS) isoforms have been localized to the kidney (1), and intrarenal inhibition of NOS has been shown to increase blood pressure (32). NOS1 (neuronal NOS) is predominantly localized in the macula densa, neurons, Bowman's capsule, and collecting duct, where it participates in the control of glomerular hemodynamics, renin release, and sodium excretion (1,24,46). Expression of NOS2 (inducible NOS) protein has been difficult to reproducibly detect in the normal kidney; however, there appears to be NOS2 mRNA in the medullary thick ascending limb (34). NOS3 (endothelial NOS) is localized in vascular endothelial cells and tubules, where it is important in the maintenance of glomerular filtration rate, vascular tone, and...

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confidence: 75%

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confidence: 99%

Renal NOS activity, expression, and localization in male and female spontaneously hypertensive rats

Sullivan

Pardieck

Hyndman

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…[16][17][18] Regarding the kidney, elevation of plasma renin level begins at age 18 weeks 19) and disturbance of renal function from 22-24 weeks. 20) Although many attempts have been made at treating SHRsp with ARBs or CCBs, treatment was often performed before the appearance of hypertensive disorders, and it remains unknown whether these drugs exert renoprotective effects when they administered after the onset of kidney disease.…”

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confidence: 99%

Renoprotective Effect of Azelnidipine in Rats

Kurashige

Abe

Furusu

et al. 2008

Biological & Pharmaceutical Bulletin

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To assess whether azelnidipine (AZN) exerts renoprotective effects, 20-week-old adult male stroke-prone spontaneously hypertensive rats (SHRsp) were treated with AZN 10 mg/kg/d (n‫,)6؍‬ olmesartan (OLM) 3 mg/kg/d (n‫,)4؍‬ hydralazine (HYD) 20 mg/kg/d (n‫,)3؍‬ or water (control; n‫.)5؍‬ Each test agent was administered by oral gavage for 12 weeks. Systolic blood pressure (SBP) was measured every 2 weeks and urinary protein excretion (UproV) every 3 weeks. At the age of 32 weeks, the rats were sacrificed and blood and kidneys collected for biochemical, histological, and immunohistochemical studies. All drug treatments significantly (pϽ0.05) reduced SBP, UproV, and blood biochemical parameters such as creatinine, total cholesterol, and blood urea nitrogen. Masson trichrome staining and immunohistochemical staining revealed significant (pϽ0.05) reductions of interstitial fibrosis, collagen type III, nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide phosphate oxidase, and p22 phox and p47 phox components expression in the AZN-and OLM-treated groups in comparison with rats treated with HYD and control animals. ED1, 4-hydroxy-2-nonenal (4-HNE), and heat shock protein (HSP)-47 expression was also reduced in the AZN-and OLM-treated groups versus in HYD and control animals. These results indicate that not only OLM but also AZN exerts renoprotective effects through inhibition of macrophage infiltration and antioxidant activity in SHRsp model of renal injury.

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“…In the present study, we evaluated the renoprotective effects of 2-wk administration of ANG-(1-7) in the stroke-prone spontaneously hypertensive rat (SHRSP) with moderate load of NaCl, a model of severe arterial hypertension associated with nephropathy and insulin resistance (11,33,54). We particularly focused on renal effects of ANG-(1-7) treatment at various levels such as inflammation markers (tissue levels of TNF-␣, NF-B, and IL-6), structural modifications (fibrosis and glomerular abundance of nephrin), and functional effects (proteinuria, creatinine clearance, and arterial blood pressure).…”

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Angiotensin-(1–7) reduces proteinuria and diminishes structural damage in renal tissue of stroke-prone spontaneously hypertensive rats

Giani

Muñoz

Pons

et al. 2011

American Journal of Physiology-Renal Physiology

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Gender-related differences in advanced glycation endproducts, oxidative stress markers and nitric oxide synthases in rats

Cited by 55 publications

References 39 publications

Renal NOS activity, expression, and localization in male and female spontaneously hypertensive rats

Renal NOS activity, expression, and localization in male and female spontaneously hypertensive rats

Renoprotective Effect of Azelnidipine in Rats

Angiotensin-(1–7) reduces proteinuria and diminishes structural damage in renal tissue of stroke-prone spontaneously hypertensive rats

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