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    Benserazide Applications Cause to the Hypertension in Salt Loaded Rats
    (Wiley-Blackwell, 2015) Aksulu, Hakki Engin; Akdur, Secil; Gungor, Buket; Sılan, Coşkun
    [Anstract Not Available]
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    Buthionine Sulfoximine (BSO) Applications Decrease Sodium Clearance and Cause to the Development of the Hypertension in Rats Treated with Low Doses of N-Nitro-L-Arginine (L-NNA)
    (Wiley-Blackwell, 2015) Aksulu, Hakki Engin; Sılan, Coşkun; Gungor, Buket; Akdur, Secil
    [Anstract Not Available]
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    Öğe
    Changes of the Renal Dopaminergic Activity during the Hypertension Generation with L-NNA Application and Salt Load in Rats
    (Wiley-Blackwell, 2015) Aksulu, Hakki Engin; Sılan, Coşkun; Gungor, Buket; Akdur, Secil
    [Anstract Not Available]
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    Effects of Resveratrol on Hypertension Developing by NOS inhibition
    (Wiley-Blackwell, 2015) Aksulu, Hakki Engin; Sılan, Coşkun; Gungor, Buket; Akdur, Secil
    [Anstract Not Available]
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    Intensive Exercise Developt Hypertension in Rats Fed with High Salty Diet
    (Wiley-Blackwell, 2015) Sılan, Coşkun; Gungor, Buket; Akdur, Secil; Aksulu, Hakki Engin
    [Anstract Not Available]
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    Resveratrol did not alter blood pressure in rats with nitric oxide synthase-inhibited hypertension
    (Clinics Cardive Publ Pty Ltd, 2017) Aydin, Mehmet; Gungor, Buket; Akdur, A. Secil; Aksulu, Hakki Engin; Sılan, Coşkun; Susam, Ibrahim; Cabuk, Ali Kemal
    Background: Inhibition of nitric oxide synthase (NOS) is a well-known experimental model of hypertension (HT). It was shown that oxidative stress contributes to the pathogenesis of HT. Resveratrol is a potent anti-oxidant that is found in red grapes, peanuts and red wine. It improves the NO response and increases endothelial NOS expression, which causes endothelium-dependent vasorelaxation as well as renal vasodilation. We aimed to explore the effects of resveratrol on blood pressure, the water-salt balance and sodium excretion as a reflection of renal function in NOS-inhibited rat models. Methods: Thirty-five male Sprague-Dawley rats (200-250 g) were used in this study. In order to obtain hypertension models, an NOS inhibitor, N-nitro-L-arginin (L-NNA) was used. The rats were randomly divided into five groups: controls (given water and 0.8% salty diet) and four groups [given L-NNA, resveratrol (RSV) eluent, RSV, and L-NNA + RSV]. Blood pressures were measured indirectly by the tail-cuff method on the first, seventh and 10th days. At the end of the study protocol (10th day), fluid balance, glomerular filtration rate, fractional sodium excretion, and blood and urine sodium and creatinine levels were measured. Results: At the end of the study protocol, blood pressures were higher in only the L-NNA group (117.8 +/- 3.5 vs 149.5 +/- 2.1 mmHg; p < 0.05), as expected. Additional applications of RSV with L-NNA could not prevent the increase in blood pressure (122.8 +/- 7.3 vs 155.4 +/- 4.4 mmHg; p < 0.05). There were no remarkable changes in water-salt balance and renal function with the application of resveratrol. Conclusion: Resveratrol was unable to prevent or reverse blood pressure increase in NOS-inhibited rats.
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    Salt and Nitric Oxide Inhibition Induced Hypertension: The Role of Prostacycline and 8-Isoprostane
    (Taylor & Francis Inc, 2011) Ilhan, Selcuk; Oktar, Suleyman; Sahna, Engin; Aksulu, Hakki Engin
    Renal prostacycline (PGI(2)) and oxidative stress are known to be important factors that effect the natriurezis and diuresis. 8-iso prostaglandin F-2 alpha (8-isoprostane), a member of F-2-isoprostanes, is formed from the nonenzymatic reaction of arachidonic acid and oxygen radicals in vivo and in vitro, and also it is a marker of oxidative stress in vivo. The aim of this study is to determine the role of renal PGI(2) and 8-isoprostane in a salt and nitric oxide (NO) inhibition-induced hypertension model. Rats were distributed equally among four groups (n = 6 per group). Control rats were given normal salt diet (0.32%); high-salt (HS) rats were given high salt diet (3.2%); NG-nitro-L-arginine (L-NNA) rats were given normal salt diet and 25 mg/kg L-NNA; HS+L-NNA rats were given high salt diet and 25 mg/kg L-NNA. Rats were placed in individual metabolic cages for 17 days. Systolic blood pressure (SBP) was measured at days initial, 7th and 14th. Urinary 8-isoprostane and PGI(2) levels were analyzed. Salt-loading alone did not change SBP values. The average SBP in L-NNA and HS+L-NNA groups were shown to significantly enhance compared to initial and day 7th in the same groups, respectively. The levels of 8-isoprostane in the HS+L-NNA group was significantly enhanced compared to the other groups. L-NNA or HS diet alone did not change the levels of 8-isoprostane compared to the control group. L-NNA alone did not change PGI(2) levels in urine compared to the control. PGI(2) levels in the HS, and the HS+L-NNA group was significantly higher compared to the control group. This study concluded that NOS inhibition plus salt-loading induced oxidative stress and increased renal PGI(2). Also, it is suggested that augmented oxidative stress may aggravate the hypertension. But the renal synthesis of PGI(2) is increased in order to augment the diuresis and natriuresis without the effect of blood pressure (BP).