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    Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells
    (Taylor & Francis Inc, 2007) Erol, Ayse; Cinar, Mehtap G.; Can, Cenk; Murat, Olukman; Uelker, Sibel; Kosay, Sezen
    Hyperhomocysteinemia is widely recognized as an independent risk factor for coronary artery vascular disease, although the underlying mechanisms are not well understood. This study aims to investigate the effect of homocysteine on nitric oxide ( NO) production in coronary microvascular endothelial cells (CMECs) and putative mechanisms mediating this effect. CMECs were isolated on Langendorff system by collagenase perfusion of hearts from male rats and cultured. The effect of homocysteine (0.01 to 1 mM) on basal and stimulated NO production was evaluated by measuring nitrite in the culture media after incubation with or without N-G-nitro-L-arginine methyl ester (L-NAME) ( 1 mM), superoxide dismutase (100 U/mL), or catalase ( 1000 U/mL) for 24 h. Total nitrite was measured using Griess reaction after reduction of nitrate to nitrite with nitrate reductase. Homocysteine did not affect basal nitrite accumulation; however, it significantly increased the nitrite accumulation induced by the calcium ionophore A23187 or interleukin-1 beta only at 1 mM. This effect of homocysteine was significantly inhibited by L-NAME, superoxide dismutase, and catalase. In conclusion, homocysteine increases NO release from stimulated CMECs without affecting basal NO production, which is probably accompanied by increased production of reactive oxygen species. It can be postulated that endothelial cells generate NO in order to minimize the damage caused by homocysteine.
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    Nitric oxide does not downregulate Rho-kinase (ROCK-2) expression in rat coronary endothelial cells
    (Lippincott Williams & Wilkins, 2008) Tiftik, R. Nalan; Erol, Ayse; Cinar, Mehtap G.; Kubat, Havva; Ark, Mustafa; Ulker, Sibel; Buyukafsar, Kansu
    Rho kinase (ROCK) and nitric oxide (NO) are important targets in cardiovascular diseases. Therefore, we investigated the possible influence of NO on Rho kinase (ROCK-2 isoform) expressions in cultured rat coronary microvascular endothelial cells. The cells were isolated from Wistar rats on a Langendorff system, and were incubated overnight (similar to 16 h) with an NO generator, A-23187 (10(-7) to 10(-6) M) NO donors, such as sodium nitroprusside (10(-7) to 10-6 M) glyceryl trinitrate (10(-7) to 10-6 M), 2,2'-(hydroxynitro- sohydrazono)bis-ethanimine (10(-7) to 10(-6) M), and NaNO2 (10(-4) to 10(-3) M) or a nitric oxide synthase (NOS) inhibitor, N-G-nitro-L-arginme methylester (2x10(-4) M), or two ROCK inhibitors, (-+)(R)-trans-4-(1-aminoethyl)- N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride monohydrate (Y-27632, 10(-5) M) and fasudil (10(-5) M) in the absence or presence of thrombin (4 U/mL). ROCK-2 and endothelial NOS (eNOS) expressions were detected by Western blotting. Moreover, nitrite/nitrate levels were detected by Griess method in the presence of the ROCK inhibitors. The NO donors and the NO generator had no significant effects on ROCK-2 expression. Y-27632 and fasudil did not alter eNOS expression and NO production. Nitrite/nitrate levels were 4.4 +/- 0.32 mu M in control and 4.0 +/- 0.93 mu M and in Y-27632 group. These results demonstrate that prolong NO donation could not suppress the expression of ROCK-2 protein, and the ROCK inhibitor did not change e-NOS expression and NO production in the cultured rat coronary microvascular endothelial cells.
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    Pharmacologic targets on the female urethra
    (Karger, 2008) Canda, A. Erdem; Cinar, Mehtap G.; Turna, Burak; Sahin, M. Oguz
    Introduction: This article reviews the mechanisms affecting contraction and relaxation of the urethra in order to establish a basis for current and future treatments for urinary incontinence in women. Material and Methods: A review of the English literature using MEDLINE was performed between 1970 and 2008 on female urethra pharmacology, urinary incontinence, and mechanisms involved in contraction and relaxation of the female human urethra. Results: alpha - Adrenoceptors (ARs) cause contraction and beta-ARs cause relaxation. Use of selective alpha - agonist and beta-AR blocker agents might have potential for the treatment of stress urinary incontinence. Tolerable doses of cholinergic agonists did not have significant effects on intraurethral pressure. Nitric oxide seems to be the major nonadrenergic- noncholinergic inhibitory transmitter causing relaxation. c-kit-positive interstitial cells seem to regulate urethral tone. The roles of adenosine triphosphate and carbon monoxide have not been fully investigated in humans. Neuropeptides function similarly to the urinary bladder. Prostanoids cause urethral contraction and relaxation depending on their subtypes. Serotonin enhances the strength of urethral sphincteric contractions. The Rho- kinase pathway also appears to be modulating smooth muscle contraction in the urethra. Conclusions: Understanding of the urethral function and pharmacology may lead to the development of promising new agents which might be useful in the management of urinary incontinence in women. Copyright (c) 2008 S. Karger AG, Basel
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    Role of Rho-kinase in contractions of ureters from rabbits with unilateral ureteral obstruction
    (Mary Ann Liebert Inc, 2007) Turna, Burak; Cinar, Mehtap G.; Canda, Erdem A.; Semerci, Bulent; Orhan, Elif C.; Tiftik, Nalan R.; Nazli, Oktay; Buyukafsar, Kansu
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    Role of Rho-kinase in contractions of ureters from rabbits with unilateral ureteric obstruction
    (Blackwell Publishing, 2007) Turna, Burak; Cinar, Mehtap G.; Canda, Abdullah E.; Orhan, Elif C.; Tiftik, Nalan R.; Nazli, Oktay; Buyukafsar, Kansu
    To investigate the expression of two isoforms of Rho-kinase (ROCK) and its functional role in the pathophysiological control of smooth muscle contraction in rabbits with unilateral ureteric obstruction (UUO). Left UUO was created in 14 rabbits and eight other rabbits (controls) had sham operations. After 2 weeks all the rabbits were killed. Ureteric strips suspended in an organ bath were used for functional studies and the effects of Y-27632, a specific inhibitor of Rhokinase, on spontaneous contractions and electrical field stimulation (EFS; 50 V, 1 ms, 16 Hz, for 20 s), carbachol- (10(-7) - 10(-4) M), phenylephrine- (10(-7) - 10(-4) M) and KCl- (50 mM) induced contractions were analysed. Western blotting was used to determine expression levels of Rho-kinase protein in the ureters of UUO and control rabbits. In the functional analysis, the contractions induced by EFS, KCl, phenylephrine and carbachol in the ureteric strips from rabbits with UUO were significantly greater than those from the control rabbits. Y-27632 considerably suppressed the ureter contractile responses in both UUO and control rabbits. Western blot analysis showed that both ROCK-1 and ROCK-2 proteins were expressed in the rabbit ureter. In accordance with the functional studies, the expression levels of both ROCK-1 and ROCK-2 were significantly greater in the ureters of UUO rabbits than in the controls. Y-27632 suppressed ureteric contractions in the rabbits with UUO. Western blot analysis also confirmed greater expression levels of ROCK-1 and ROCK-2 in the ureters of UUO rabbits. It is important to elucidate by which mechanisms the Rho-kinase pathway affects ureteric function after obstruction.