Preconditioning protects endothelium by preventing ET-1-induced activation of NADPH oxidase and xanthine oxidase in post-ischemic heart

Duda, Monika; Konior, Anna; Klemenska, Emilia; Beresewicz, A

doi:10.1016/j.yjmcc.2006.10.014

Cited by 44 publications

(40 citation statements)

References 43 publications

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“…Currently, all available evidence related to COPD mechanisms firmly suggests that oxidative stress plays a significant role in the pathogenesis of COPD [6]. ET-1 stimulates the production of superoxide via NADPH oxidase activation, and, conversely, reactive oxygen species appear to stimulate ET-1 production [36]. The prevention of decrease in antioxidant activity upon intervention with ET-1 receptor antagonists suggests that ET-1 is involved in the pathophysiological pathway of oxidative stress in the development of emphysema.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

Chen

Hanaoka²,

Droma³

et al. 2009

Eur Respir J

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We hypothesised that endothelin (ET)-1 plays an important role in the pathogenesis of emphysema. We attempted to apply ET-1 receptor antagonists to demonstrate and further elucidate the molecular pathogenesis pathways through which ET-1 may cause emphysematous changes.Sprague-Dawley rats were divided into four groups: control, cigarette smoke extract (CSE), CSE+BQ-123 (a selective endothelin receptor type A (ET A ) antagonist) and CSE+bosentan (a mixed ET A /ET B receptor antagonist). The CSE was injected intraperitoneally once a week for 3 weeks, and BQ-123 or bosentan was administered daily for the same duration. The expression of ET A receptor, apoptosis index, caspase-3 activity, matrix metalloproteinase (MMP)-2 and MMP-9 activity, and tumour necrosis factor (TNF)-a and interleukin (IL)-1b concentrations were measured in the lung tissue. The ET-1 levels and antioxidant activity were measured in the serum.Both BQ-123 and bosentan prevented the development of CSE-induced emphysema, blocked the expression of ET A receptor, inhibited pulmonary apoptosis, inactivated MMP-2 and MMP-9 activities in the lung tissues, reduced the concentrations of inflammatory cytokines TNF-a and IL1b, and improved the biological antioxidant activity in the serum.Emphysema development is suppressed by ET-1 receptor antagonists. ET-1 may cause emphysematous changes through molecular pathogenesis pathways involving apoptosis, proteinase and antiproteinase imbalance, inflammation and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

Chen

Hanaoka²,

Droma³

et al. 2009

Eur Respir J

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“…The results from that study indicated corresponding increases in mast cell secretory products (i.e., histamine or tumor necrosis-␣) in response to oxidants perfused through isolated hearts and that mast cell stabilizers blocked this release. More recent reports have demonstrated that treatment of ischemic myocardium with either selective (ET A , BQ-123) or nonselective (ET A -ET B , bosentan) receptor antagonism significantly reduced catalase and superoxide dismutase activity as well as glutathione content (20,27,41). Indeed, our preliminary data (n ϭ 3/group) reveals a significant reduction in the LV tissue levels of malonyl-CoA dehydrogenase at 3 days postsurgery in ETA-treated fistula animals compared with untreated fistula values (791 Ϯ 72 vs. 1,380 Ϯ 168 nM malondialdehyde/wet LV tissue weight, Fist ϩ ETA vs. Fist respectively, P Յ 0.05).…”

Section: Effect Of Et a Receptor Antagonism On Postfistula Remodelingmentioning

confidence: 97%

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

Murray¹,

McMillan²,

Brower³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Murray DB, McMillan R, Brower GL, Janicki JS. ETA selective receptor antagonism prevents ventricular remodeling in volume-overloaded rats. Am J Physiol Heart Circ Physiol 297: H109 -H116, 2009. First published May 8, 2009 doi:10.1152/ajpheart.00968.2008.-The objective of this study was to investigate the ability of selective endothelin receptor subtype A (ET A) endothelin receptor antagonism (ETA) to prevent the acute myocardial remodeling process secondary to volume overload. Left ventricular tissue from sham-operated (Sham) and untreated (Fist), and TBC-3214 (Fist ϩ ETA, 25 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 )-treated fistula animals was analyzed for mast cell density, matrix metalloproteinase (MMP) activity, and extracellular collagen volume fraction (CVF) 1 and 5 days following the initiation of volume overload. Compared with Fist, ETA treatment prevented the increase in left ventricular mast cell density at 1 day and 5 days. Additionally, at 1 day postfistula, a substantial decrease in MMP-2 activity below Sham levels was observed following endothelin receptor antagonism (1.7 Ϯ 0.7 vs. 0.3 Ϯ 0.3 vs. 0.9 Ϯ 0.2 arbitrary activity units, Fist vs. Fist ϩ ETA vs. Sham, P Յ 0.05). This same effect was also seen at 5 days postfistula (1.9 Ϯ 0.3 vs. 0.5 Ϯ 0.1 arbitrary activity units, Fist vs. Fist ϩ ETA, P Յ 0.05). The marked decrease in myocardial CVF seen in Fist hearts (0.7 Ϯ 0.1 vs. 1.6 Ϯ 0.1% myocardial area, Fist vs. Sham, P Յ 0.05) was prevented by ETA (1.7 Ϯ 0.1% Fist ϩ ETA, P Ͻ 0.05 vs. Fist). This preservation of the collagen matrix was also present on day 5 in the TBC-treated group vs. the Fist group (1.0 Ϯ 0.1 vs. 1.4 Ϯ 0.1%, Fist vs. Fist ϩ ETA, P Յ 0.01). Furthermore, an 8-wk preventative treatment with ETA significantly attenuated the increase in left ventricular end systolic and diastolic volumes compared with untreated fistula hearts. In conclusion, the novel findings of this study indicate that the activation of cardiac mast cells and subsequent MMP activation/collagen degradation during the acute stages of volume overload are prevented by blockade of the ET A receptor subtype. Furthermore, by preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits.endothelin-1; mast cell; matrix metalloproteinase; TBC-3214 ENDOTHELIN (ET)-1 is a potent neurohormone produced throughout the cardiovascular system, and the observation that plasma ET-1 is elevated in patients with heart failure is suggestive of a role in the pathophysiology of heart failure (16,19,34,40,47). The cardiovascular effects of ET-1 (a 21-amino-acid peptide) are dictated by binding to one of two G protein-linked receptor subtypes [endothelin receptor subtypes A (ET A ) or B (ET B )] (23). In the heart and vasculature, binding and activation of ET A is known to mediate powerful vasoconstrictor and pressor affects, in addition to chronotropic and ionotropic effects (12,25). The ET B receptor subtype is responsible for systemic clearance of circulating ...

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“…In the fourth protocol, the HKS-induced constrictions of the epineurial arterioles were studied in the absence and presence of SOD (120 U/ml) alone, catalase alone (5,000 U/ml), SOD (120 U/ml) plus catalase (5,000 U/ml), tempol (a cell membrane-permeable superoxide scavenger; 10 Ϫ4 M) (8) In the fifth protocol, the effects of N -nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthase; 10 Ϫ6 -3 ϫ 10 Ϫ5 M) on changes in the diameter of epineurial arterioles were studied under LKS conditions. Additionally, in the presence of L-NAME (10 Ϫ5 M), the effects of S-nitroso-N-acetylpenicillamine (SNAP, an NO donor; 10 Ϫ9 -10 Ϫ6 M) on changes in the diameter of epineurial arterioles were studied under LKS conditions.…”

Section: Methodsmentioning

confidence: 99%

High oxygen tension constricts epineurial arterioles of the rat sciatic nerve via reactive oxygen species

Sakai

Mizuno²,

Ono³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Sakai N, Mizuno R, Ono N, Kato H, Ohhashi T. High oxygen tension constricts epineurial arterioles of the rat sciatic nerve via reactive oxygen species. Am J Physiol Heart Circ Physiol 293: H1498-H1507, 2007. First published May 18, 2007; doi:10.1152/ajpheart.01190.2006.-Microcirculation of the sheath of the rat sciatic nerve fiber was investigated by using an intravital microscope, and changes in the diameter of the epineurial arterioles in response to highly oxygenated Krebs-bicarbonate solution were evaluated. Superfusion of low-oxygen (0%) Krebs-bicarbonate solution (LKS) onto rat sciatic nerves did not affect changes in the diameter of the arterioles. Nifedipine, a Ca 2ϩ -channel blocker, caused a dosedependent dilation of the epineurial arterioles in LKS. In contrast, superfusion of high-oxygen (21%) Krebs-bicarbonate solution (HKS) onto rat sciatic nerves significantly constricted the epineurial arterioles in a time-dependent manner. The HKS-induced constriction of the epineurial arterioles was significantly reduced by treatment with 120 U/ml superoxide dismutase (SOD) alone or 5,000 U/ml catalase alone. In the presence of 120 U/ml SOD plus 5,000 U/ml catalase, 10 Ϫ4 M tempol, 10 Ϫ6 M diphenyleneiodium, 2 ϫ 10 Ϫ4 M apocynin, or 10 Ϫ6 M allopurinol, the HKS-induced constriction of the epineurial arterioles completely disappeared. These results suggest that superfusion of highly oxygenated solution onto rat sciatic nerves constricts the epineurial arterioles through reactive oxygen species (ROS), including superoxide and hydrogen peroxide, and that production of superoxide involves a NADPH oxidase-or xanthine oxidase-dependent pathway. In conclusion, ROS play significant roles in the regulation of microcirculation of rat sciatic nerves in vivo. peripheral nerves; microcirculation; superoxide; hydrogen peroxide BLOOD SUPPLY TO PERIPHERAL nerves is important to maintain the functions of the nerve fibers. The disturbance of blood circulation within sciatic nerves produces dysfunction such as suppression of motor nerve conduction velocity (2, 3). It has become clear that pathogenesis of diabetic neuropathy is associated with a reduction of blood flow in sciatic nerves in diabetic animals and humans (14, 34). Thus understanding the regulation of blood flow in sciatic nerves is quite important for diagnosis and treatment of diabetic neuropathy.Laser Doppler flowmetry and hydrogen clearance are methods available to study the blood flow in sciatic nerves in vivo (2-4, 16, 17, 30, 33, 35, 46). From the use of these methods, it is known that the epineurial and endoneurial arterioles of sciatic nerves play crucial roles in the regulation of microcirculation. Although these methods are capable of measuring local blood flow in the sheath of sciatic nerves in vivo, changes in the diameter of the arterioles in the sheath of sciatic nerves could not be identified. It is necessary to measure changes in the diameter of the arterioles in vivo, because the arterioles and small arteries are resistant vessels, and changes in the...

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Preconditioning protects endothelium by preventing ET-1-induced activation of NADPH oxidase and xanthine oxidase in post-ischemic heart

Cited by 44 publications

References 43 publications

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

High oxygen tension constricts epineurial arterioles of the rat sciatic nerve via reactive oxygen species

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Preconditioning protects endothelium by preventing ET-1-induced activation of NADPH oxidase and xanthine oxidase in post-ischemic heart

Cited by 44 publications

References 43 publications

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

Endothelin-1 receptor antagonists prevent the development of pulmonary emphysema in rats

ETAselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

High oxygen tension constricts epineurial arterioles of the rat sciatic nerve via reactive oxygen species

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ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats