NORMOTENSIVE RATS WITH PCOS EXHIBIT THE HYPERTENSIVE PATTERN: FOCUS ON OXIDATIVE STRESS

Reproduction ◽  
2021 ◽  
Author(s):  
Jovana Joksimovic Jovic ◽  
Nikola Jovic ◽  
Jasmina Sretenovic ◽  
Vladimir Zivkovic ◽  
Maja Nikolic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulse Pressure ◽  
Polycystic Ovary ◽  
Strain Differences ◽  
Reproductive Age ◽  
Subcutaneous Injections ◽  
Ovarian Volume ◽  
Spontaneously Hypertensive ◽  
Ovarian Morphology ◽  
Wistar Kyoto

Numerous evidence implies complex interrelations between polycystic ovary syndrome (PCOS) and hypertension (HT) in reproductive-age women. We aimed to investigate the potential strain differences in ovarian morphology, hemodynamic and biochemical characteristics in an androgen-induced PCOS rat model. A total of 3 weeks old 24 rats (12 Wistar Kyoto - WK and 12 Spontaneously Hypertensive Rats – SHR) were divided into four groups: WK, WK PCOS, SHR, and SHR PCOS. PCOS was induced by daily subcutaneous injections of testosterone-enanthate (1 mg/100 g body weight (BW)) administered for 5 weeks. PCOS induction led to estrus cyclicity cessation, cystic ovarian appearance, and sex hormones disturbances in both strains. The morphometric parameters in ovaries were altered in a manner of PCOS-related changes in both strains (higher number in preantral, atretic and cystic follicles). Ultrasonographycally, a significant decrease in ovarian volume (OV) was registered in PCOS groups, but also in SHR compared to WK rats. All blood pressure parameters were higher in SHR compared to WK. PCOS modeling increased systolic, mean arterial and pulse pressure in WK strain, while in SHR, only mean arterial and pulse pressure were higher. Alterations in oxidative stress parameters could provide a molecular basis for PCOS-related changes: in PCOS groups, TBARS and O2- were higher in both strains, while SOD and GSH were significantly lowered.

scholarly journals Polycystic ovarian morphology in Thai women of reproductive age with polycystic ovary syndrome

2020 ◽  
Vol 14 (6) ◽  
pp. 271-277
Author(s):  
Thanyarat Wongwananuruk ◽  
Panicha Chantrapanichkul ◽  
Vichuta Unalome ◽  
Suchada Indhavivadhana ◽  
Manee Rattanachaiyanont ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Testosterone Level ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Women Of Reproductive Age ◽  
Ovary Syndrome ◽  
Ovarian Volume ◽  
Thai Women ◽  
Tertiary Teaching ◽  
Ovarian Morphology

AbstractBackgroundAdvancements in ultrasound technology have facilitated identifying polycystic ovarian morphology (PCOM) in women with and without polycystic ovary syndrome (PCOS), but it still has limitations due to follicle counting methods and variation of phenotypes according to ethnicity. Ethnicity-specific ovarian morphology may help to establish ethnicity-specific follicle count cut points for defining PCOM in women with PCOS.ObjectivesTo investigate the prevalence and factors associated with PCOM in Thai women of a reproductive age with PCOS.MethodsThis prospective cross-sectional study was conducted in our gynecology department at a tertiary teaching hospital from February 2016 to May 2017. We included women with PCOS, who were measured for weight, height, waist circumference, and blood pressure. Blood samples were taken to measure fasting blood glucose, lipid profile, testosterone level, and 2 h post-load 75 g oral glucose tolerance test (OGTT). Transvaginal or transrectal sonography was performed to evaluate their ovaries.ResultsAll 143 patient participants we included had oligomenorrhea, 77.6% of them had acne, and 64.3% hirsutism. Their average total testosterone level was 0.47 ± 0.10 ng/mL. The prevalence of PCOM was 55.2%. The proportions of PCOM diagnosed by ovarian follicle and ovarian volume criteria were 36.4% and 42.0%, respectively. There were 20.0 ± 9.5 follicles per ovary, 8.3 ± 3.1 follicles per cross section, and the mean ovarian volume was 7.9 ± 3.0 mL.ConclusionThe overall prevalence of PCOM in Thai women of reproductive age with PCOS was 55.2%. Our univariate analysis found no factors significantly associated with PCOM.

Effect of resveratrol administration on ovarian morphology, determined by transvaginal ultrasound for the women with PCOS

2021 ◽  
pp. 1-18
Author(s):  
Amir Pejman Hashemi Taheri ◽  
Behnaz Moradi ◽  
Amir Reza Radmard ◽  
Milad Sanginabadi ◽  
Mostafa Qorbani ◽  
...  
Keyword(s):  
Repeated Measures ◽  
Polycystic Ovary ◽  
Transvaginal Ultrasound ◽  
Antral Follicle ◽  
Antral Follicle Count ◽  
Ovarian Volume ◽  
Exact Test ◽  
Ovarian Morphology ◽  
The Mean

Abstract Background: Intake of resveratrol has been associated with improved ovarian morphology under in vitro and in the animal models; however, this finding has not been confirmed in trials. The aim of our study was, therefore, to use a placebo-controlled approach with the detailed assessment of the ovarian morphology by applying transvaginal ultrasound to examine the effectiveness of this therapeutic approach in this group of women. Methods: Forty-one women with polycystic ovary syndrome (PCOS) were randomly assigned (1:1) to 3 months of daily 1000 mg resveratrol or placebo. Random assignment was done by blocked randomisation. Our primary endpoints were the change in the ovarian volume, stromal area and antral follicle count per ovary (FNPO) from the baseline to 3 months. Secondary endpoints were improvement in the distribution of follicles and ovarian echogenicity. Differences between the resveratrol and control groups were evaluated by Chi-square, fisher’s exact test and repeated-measures of ANOVA. Results: The mean age of all participants was 28.61 ± 4.99 years, with the mean BMI of 28.26 ± 5.62 kg/m2. Resveratrol therapy, as compared with placebo, was associated with a significantly higher rate of improvement in the ovarian morphology (p= 0.02). Women who received resveratrol had a more dominant follicle than those getting placebo, with a significant reduction in the ovarian volume (p<0.05). However, the number of FNPO, stromal area, ovarian echogenicity and distribution of follicles were not significantly altered (P>0.05). Conclusions: Treatment with resveratrol significantly reduced the ovarian volume and PCOM, thus suggesting a disease-modifying effect in PCOS. Trial registration: IRCT, IRCT2017061917139N2. Registered 7 July 2017, http://irct.ir/trial/15836.

Acute renal denervation produces a diuresis and natriuresis in young SHR but not WKY rats

1986 ◽  
Vol 251 (4) ◽  
pp. F655-F661 ◽  
Author(s):  
M. A. Rudd ◽  
R. S. Grippo ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Strain Differences ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Clearance experiments were conducted to determine the effect of acute unilateral renal denervation (DNX) on renal hemodynamics and salt and water excretion in anesthetized 6-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto genetic control rats (WKY). Before DNX, SHR had higher mean arterial pressure (33%) and renal vascular resistance (RVR) (57%) and lower glomerular filtration rate (GFR) (10%); urine flow and sodium excretion were similar. Following DNX in SHR, sodium and water excretion increased by 138 and 62%, respectively (P less than 0.001); GFR and RVR were unchanged. In contrast, DNX in WKY did not affect urine flow (0%) or sodium excretion (-21%). These strain differences were observed in Okamoto-Aoki rats from two sources. Effective DNX was indicated by 95% reduction of norepinephrine content 3 days after DNX in both strains. Six-week-old Sprague-Dawley and Munich-Wistar rats, in contrast to WKY, responded to DNX with a natriuresis (+182%) and diuresis (+95%) (P less than 0.001). Renal function was unaffected by sham DNX in SHR. Our results indicate that efferent renal nerve activity has little tonic influence on the renal vasculature in these young rats. Augmented neurotransmitter release and/or tubular responsiveness may be involved in fluid and electrolyte retention and the pathogenesis of hypertension in SHR. Conversely, blunted renal neuroeffector responses may prevent WKY from developing hypertension.

Dissociation between vascular oxidative stress and cardiovascular function in Wistar Kyoto and spontaneously hypertensive rats

2006 ◽  
Vol 45 (2) ◽  
pp. 112-121 ◽  
Author(s):  
Pierre Sicard ◽  
Alexandra Oudot ◽  
Jean-Claude Guilland ◽  
Daniel Moreau ◽  
Catherine Vergely ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spontaneously Hypertensive Rats ◽  
Cardiovascular Function ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Vascular Oxidative Stress

scholarly journals Roles of Oxidative Stress in Policystic Ovary Syndrome

2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Marija Bicanin Ilic ◽  
Aleksandra Dimitrijevic ◽  
Igor Ilic
Keyword(s):  
Oxidative Stress ◽  
Polycystic Ovary ◽  
Signs And Symptoms ◽  
Reproductive Age ◽  
The Novel ◽  
Ovary Syndrome ◽  
Total Antioxidative Capacity ◽  
Definition Of ◽  
Insuline Resistance ◽  
Oxidative Biomarkers

Abstract Polycystic ovary syndrome (PCOS) represent a common endocrine disorder that affects nearly 4 to 12 percents of reproductive age women in general population studies (1). PCOS is caracterized by the oligoovulation or anovulation, hyperandrogenisam and multiple small ovarian cysts. The etiology of PCOS is steel unclear. Patophysiology of PCOS represents the complex mehanism. There is a wide spectar of signs and symptoms of the PCOS, which vary in severity over the time and within individuals. Major symptoms are: the amenhorhea, oligomenorhea combined with of episodes of menometrorhagia. Some signs of hiperandrogenism are: acne, hirsutism and alopecia. Other important symptoms of the PCOS are: the obesity, dyslpedemia, insuline resistance, metabolic syndrome, infertility, endometrial neoplasia, pregnancy loss. Diagnosis is achieved by exclusion of other factors that lead to anovulation, and laboratory assay of sex hormones and gonadotropines. One of the novel approaches in evaluation of etiology and pathogenesis of the PCOS recognizes oxidative stress as an important factor in genesis of this syndrome. For investigation of the oxidative stress role in the pathogenesis of diseases, some biochemical markers have been used including the MDA and NO also anti-oxidative biomarkers such as Total Antioxidative Capacity, Superoxide Dismutase, Glutation Peroxidase, and glutathione. Most of recent studies compared the oxidative stress biomarker level or antioxidative biomarkers levels in the PCOS patients and healthy controls. Patients with the PCOS in those studies were often subdivided in groups by the presence of insulin resistance (HOMA index) or infertility or not. One of the main problems in this field of research is inconsistency in precise definition of the PCOS, as well as different expression of various symptoms within individuals over the time. In that manner it is very difficult to follow up these patients and to establish criteria that could be compared in studies.

Options for generating polycystic ovary syndrome based on experimental findings in animal models

2020 ◽  
Vol 69 (4) ◽  
pp. 89-100
Author(s):  
Maria I. Yarmolinskaya ◽  
Elena I. Abashova ◽  
Olga L. Bulgakova
Keyword(s):  
Animal Models ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Indirect Methods ◽  
Ovulatory Dysfunction ◽  
Ovarian Morphology ◽  
Genetic Interventions ◽  
Experimental Findings

Polycystic ovary syndrome (PCOS) is a common endocrine pathology that affects 814% of women of reproductive age. The leading signs of the disease are hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. Over the past decades, a variety of animal models have been developed to study the etiology and pathogenesis of PCOS, including chemical, hormonal, and genetic interventions. However, a large number of experimental techniques differ even in the framework of a single model. In this review article, we summarized PCOS animal models using both direct hormonal effects and indirect methods.

Abnormalities in kallikrein excretion in spontaneously hypertensive rats

1985 ◽  
Vol 248 (3) ◽  
pp. F396-F403 ◽  
Author(s):  
J. L. Ader ◽  
D. M. Pollock ◽  
M. I. Butterfield ◽  
W. J. Arendshorst
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Strain Differences ◽  
Renal Perfusion ◽  
Pressure Level ◽  
Urine Flow ◽  
Analysis Of Covariance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Level Analysis

Experiments were conducted to examine kallikrein excretion in 12-wk-old anesthetized and conscious Okamoto-Aoki spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Urinary excretion of active and total kallikrein was determined at spontaneous pressures and in response to acute decreases in renal perfusion pressure (RPP; suprarenal aortic constriction). Under basal conditions, active kallikrein excretion was lower in SHR compared with WKY whether conscious (4.4 +/- 1.7 vs. 9.4 +/- 1.3 pkat . min-1 . g kidney wt-1) or anesthetized (5.7 +/- 1.3 vs. 10.4 +/- 1.7). In both anesthetized SHR and WKY, excretion of active and total kallikrein was directly related to RPP after 20 mmHg decrements in RPP and was depressed in SHR at each pressure level. The slope of the relation between active kallikrein excretion and pressure was less in SHR (0.06 +/- 0.01 vs. 0.14 +/- 0.05 pkat . min-1 . g kidney wt-1 . mmHg-1). Thus kallikrein excretion is set at a lower level in SHR and is less responsive to changes in RPP. These strain differences are not related to urine flow, Na excretion, or glomerular filtration rate (GFR) since the values were the same in both strains at each pressure level. Analysis of covariance indicated a significant correlation between active kallikrein excretion and RPP in WKY and SHR, with RPP accounting for 92% of the variation in the kallikrein data. GFR, Na excretion, and urine flow rate were not significantly correlated to active kallikrein and were responsible for only 2% of the variation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Refractory blood pressure in female SHR to increased oxidative stress is not mediated by NO or by upregulation of renal antioxidant enzymes

2010 ◽  
Vol 298 (2) ◽  
pp. R266-R271 ◽  
Author(s):  
Arnaldo F. Lopez-Ruiz ◽  
Radu Iliescu ◽  
Jane F. Reckelhoff
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Antioxidant Enzymes ◽  
Sex Difference ◽  
Spontaneously Hypertensive Rat ◽  
Pressor Response ◽  
Whole Body ◽  
Spontaneously Hypertensive ◽  
Endogenous Nitric Oxide ◽  
Wistar Kyoto

There is a sex difference in the blood pressure (BP) responses to prooxidants and antioxidants in the spontaneously hypertensive rat (SHR). In contrast to males, BP in female SHR does not decrease in response to antioxidants, such as tempol or apocynin, or increase in response to the prooxidant, molsidomine. Molsidomine decreases BP and increases expression of antioxidants in male Wistar-Kyoto rats (WKY), but not male SHR. The present study tested the hypothesis that the mechanism responsible for the lack of a pressor response to molsidomine in females is due to higher endogenous nitric oxide (NO) or to compensatory upregulation of renal antioxidant enzymes. Female SHR were treated with molsidomine in the presence or absence of nitro-l-arginine methyl ester (l-NAME) for 2 wk. Molsidomine increased nitrate/nitrite (NOx) and F2-isoprostane (F2-IsoP) excretion, whereas l-NAME reduced NOx but increased F-Isop. Molsidomine and l-NAME together further reduced NOx and increased F2-IsoP. Molsidomine alone had no effect on BP; l-NAME alone increased BP. The combination of molsidomine and l-NAME did not increase BP above l-NAME alone levels. Whole body and renal oxidative stress increased, while renal cortical Cu,Zn-SOD expression was downregulated and catalase was upregulated by molsidomine; glutathione peroxidase expression was unaffected. These data support our previous studies suggesting that BP in female SHR is independent of either increases or decreases in oxidative stress. The mechanisms responsible for the sex difference in BP response to increase or decrease of oxidative stress are not due to increased NO in females or to compensatory upregulation of antioxidant enzymes in response to increases in oxidants.

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