Immunocytochemical localization of nitric oxide synthase-III in reproductive organs of female rats during the oestrous cycle

Hyperglycemia affects male and female vascular beds differently. We have previously shown that 1 week after the induction of diabetes with streptozotocin (STZ), male and female rats exhibit differences in aortic endothelial function. To examine this phenomenon further, aortic responses were studied in male and female rats 8 weeks after the induction of diabetes (intermediate stage). Endothelium-dependent vasodilation (EDV) to acetylcholine (ACh) was measured in phenylephrine (PE) pre-contracted rat aortic rings. Concentration response curves to PE were generated before and after L-NAME, a nitric oxide synthase (NOS) inhibitor. Furthermore, mRNA expression of endothelial nitric oxide synthase (eNOS) and NADPH oxidase subunit (Nox1) were determined. At 8 weeks, diabetes impaired EDV to a greater extent in female than male aortae. Furthermore, the responsiveness to PE was significantly enhanced only in female diabetic rats, and basal NO, as indicated by the potentiation of the response to PE after L-NAME, was reduced in female diabetic rat aortae to the same levels as in males. In addition, eNOS mRNA expression was decreased, while the Nox1 expression was significantly enhanced in diabetic female rats. These results suggest that aortic function in female diabetic rats after 8 weeks exhibits a more prominent impairment and that NO may be involved.

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Hypertensive female Sprague-Dawley rats require an intact nitric oxide synthase system for compensatory increases in renal regulatory T cells

AJP Renal Physiology ◽

10.1152/ajprenal.00228.2020 ◽

2020 ◽

Vol 319 (2) ◽

pp. F192-F201

Author(s):

Lindsey A. Ramirez ◽

Ellen E. Gillis ◽

Jacqueline B. Musall ◽

Riyaz Mohamed ◽

Elizabeth Snyder ◽

...

Keyword(s):

Nitric Oxide ◽

T Cells ◽

Angiotensin Ii ◽

Nitric Oxide Synthase ◽

Regulatory T Cells ◽

Female Rats ◽

Sprague Dawley ◽

Albumin Excretion ◽

Sprague Dawley Rats ◽

Oxide Synthase

We have previously shown that hypertensive female rats have more regulatory T cells (Tregs), which contribute more to blood pressure (BP) control in female versus male rats. Based on known protective properties of Tregs, the goal of the present study was to investigate the mechanisms by which female rats maintain Tregs. The present study was designed to 1) compare the impact of three hypertension models on the percentage of renal Tregs and 2) test the hypothesis that nitric oxide synthase (NOS) inhibition prevents increases in renal Tregs and exacerbates renal damage in female Sprague-Dawley rats. Rats (11–14 wk old) were randomized to one of the following four groups: control, norepinephrine (NE) infusion, angiotensin II infusion, or the NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) in drinking water. BP was measured via tail cuff. After 2 wk of treatment, kidneys were isolated and processed to measure Tregs via flow cytometric analysis and renal injury via urinary albumin excretion, plasma creatinine, and histological analyses. Hypertensive treatments increased BP in all experimental animals. Increases in BP in norepinephrine-and angiotensin II-treated rats were associated with increases in renal Tregs versus control. In contrast, l-NAME treatment decreased Tregs compared with all groups. l-NAME treatment modestly increased albumin excretion. However, plasma creatinine was comparable among the groups, and there was no histological evidence of glomerular or tubular injury. This study provides insights into the mechanisms regulating renal Tregs and supports that an intact NOS system is crucial for female rats to have BP-related increases in renal Tregs.

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Glial and neuronal localization of neuronal nitric oxide synthase immunoreactivity in the median eminence of female rats

Brain Research ◽

10.1016/s0006-8993(97)01561-8 ◽

1998 ◽

Vol 789 (2) ◽

pp. 322-326 ◽

Cited By ~ 14

Author(s):

Shin-ichi Kawakami ◽

Masumi Ichikawa ◽

Makoto Yokosuka ◽

Hiroko Tsukamura ◽

Kei-ichiro Maeda

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Median Eminence ◽

Neuronal Nitric Oxide Synthase ◽

Female Rats ◽

Oxide Synthase

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Triiodothyronine attenuates the progression of renal injury in a rat model of chronic kidney disease

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2017-0252 ◽

2018 ◽

Vol 96 (6) ◽

pp. 603-610 ◽

Cited By ~ 1

Author(s):

Sahar M. El Agaty

Keyword(s):

Nitric Oxide ◽

Chronic Kidney Disease ◽

Nitric Oxide Synthase ◽

Kidney Disease ◽

Renal Injury ◽

Serum Levels ◽

Female Rats ◽

Renal Tubules ◽

Oxide Synthase ◽

Remnant Kidney

This study was designed to investigate whether and how triiodothyronine (T3) affects renal function in an experimental model of chronic kidney disease. Twenty-four female rats were divided into the following groups: sham-operated control group (n = 8), 5/6 nephrectomized group (Nx, n = 8), and 5/6 nephrectomized group treated with T3 for 2 weeks (T3-Nx, n = 8). T3 administration significantly decreased serum levels of urea, creatinine, tumour necrosis factorα, and interleukin-6 compared with serum levels in the Nx group. The levels of malondialdehyde, transforming growth factor β, fibronectin, and collagen IV, as well as the expression of inducible nitric oxide synthase, nuclear factor κB, poly(ADP-ribose) polymerase, caspase-3, and Bax were all significantly decreased, though not normalized, in the remnant kidney of rats in the T3-Nx group compared with Nx rats. Glutathione, heme oxygenase-1 levels, as well as endothelial nitric oxide synthase expression were increased in the remnant kidney of the T3-Nx group. Histological studies revealed focal necrosis of renal tubules associated with inflammatory cell infiltration and fibrosis in the Nx group. These changes were alleviated in T3-Nx rats. This study showed that T3 administration attenuated the clinical and histological signs of renal injury in 5/6 nephrectomized rats by mitigating renal oxidative stress, inflammation, apoptosis, and fibrosis.

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EFFECT OF RATE CORROSION OF Mg AND Mg ALLOY ON RENAL NITRIC OXIDE SYNTHASE ACTIVITY IN MALE AND FEMALE RATS

Pathophysiology ◽

10.1016/j.pathophys.2018.07.181 ◽

2018 ◽

Vol 25 (3) ◽

pp. 246 ◽

Cited By ~ 1

Author(s):

Juraj Laco ◽

Andrej Barta ◽

Marina Cebová ◽

Miroslav Čavojský ◽

František Simančík ◽

...

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Female Rats ◽

Mg Alloy ◽

Male And Female ◽

Male And Female Rats ◽

Oxide Synthase ◽

Nitric Oxide Synthase Activity

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Exercise training improves myocardial tolerance to ischemia in male but not in female rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00363.2006 ◽

2007 ◽

Vol 293 (1) ◽

pp. R363-R371 ◽

Cited By ~ 16

Author(s):

David B. Thorp ◽

James V. Haist ◽

Jennifer Leppard ◽

Kevin J. Milne ◽

Morris Karmazyn ◽

...

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Exercise Training ◽

Endothelial Nitric Oxide Synthase ◽

Diastolic Pressure ◽

Female Rats ◽

Female Rat ◽

Rat Hearts ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Acute exercise increases myocardial tolerance to ischemia-reperfusion (I-R) injury in male but not in female rat hearts, possibly due to a decreased heat shock protein 70 (Hsp70) response in the female hearts. This study examined whether repetitive exercise training would increase Hsp70 and myocardial tolerance to I-R injury in female rat hearts. Adaptations in myocardial manganese superoxide dismutase (MnSOD) and endothelial nitric oxide synthase (eNOS) were also assessed. Ten-week old male (M) and female (F) Sprague-Dawley rats ( n = 40 total) exercise-trained for 14 wk; the last 8 wk consisted of running 1 h at 30 m/min (2% incline), 5 days/wk. Following training, left ventricle mechanical function (LVMF) was monitored for 30 min of reperfusion following 30 min of global ischemia (Langendorff procedure). Myocardial Hsp70 content was not different in M and F control groups, while increases were observed in both trained groups (M greater than F; P < 0.05). Although MnSOD content did not differ between groups, endothelial nitric oxide synthase (eNOS) levels were decreased in F, with no change in M, following training ( P < 0.05). Hearts from control F demonstrated a greater recuperation of all indices of LVMF following I-R compared with control M hearts ( P < 0.05). Hearts of trained M exhibited improved recovery of LVMF (left ventricular diastolic pressure, left ventrcular end-diastolic pressure, +dP/d t, −dP/d t) during reperfusion compared with control M hearts ( P < 0.05). In contrast, hearts of trained F did not show any change in recovery from I-R. Hence, exercise training is more beneficial to M than F in improving myocardial function following I-R injury.

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