Ischemia Increases Detectable Endothelial Nitric Oxide Synthase in Rat and Human Myocardium

Bloch, Wilhelm; Mehlhorn, Uwe; Krahwinkel, Andreas; Reiner, Michael; Dittrich, M; Schmidt, Annette; Addicks, Klaus

doi:10.1006/niox.2000.0339

Cited by 58 publications

(59 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Using the preferential b 3 -adrenoceptor agonist BRL 37344, an activation of a NOS pathway has been demonstrated in human intraventricular biopsies of transplanted human myocardium, and it was suggested that the NOS isoform involved in the b 3 -adrenoceptor stimulation is probably eNOS (Gauthier et al, 1998). In the present study, we performed experiments with an anti-eNOS antibody, which has been shown previously to be specific for detection of the activated and translocated forms of eNOS (Bloch et al, 2001b;Reiner et al, 2001). Using this antibody, we observed a translocationdependent eNOS activation in human right atrial, but not in the left ventricular myocardium.…”

Section: Discussionmentioning

confidence: 87%

“…The following primary antibodies were used for immunohistochemistry: (1) rabbit anti-eNOS antibody against the bovine eNOS peptide (599-613) plus additional C-terminal Cys conjugated to KLH (PYNS-SPREQHKSYKC) (Biomol, Hamburg, Germany); this antibody has been previously shown to be specific in detecting the eNOS protein after dissociation from caveolin, that is, after translocation (Bloch et al, 2001b), anti-phospho-Akt/PKB (Upstate, Lake Placid, U.S.A.), corresponding to amino acids 301-312 of mouse pAkt/PKB, anti-phospho-eNOS Ser1177 (Upstate, Lake Placid, U.S.A.), corresponding to amino acids 1172-1183 of human eNOS and anti-phospho-eNOS Thr495 (Upstate, Lake Placid, U.S.A.), corresponding to amino acids 489-501 of human eNOS as well as anti-phospho-eNOS Ser114 corresponding to amino acids 106-118 of bovine eNOS (Upstate, Lake Placid, U.S.A.). As secondary antibodies, a biotinylated goat anti-rabbit, or biotinylated goat anti-mouse antibody (Dako, Hamburg, Germany) was used for accentuation.…”

Section: Methodsmentioning

confidence: 99%

“…This led to an augmentation of the DAF fluorescence by 32.573.0% (n ¼ 60, four experiments, Figure 1f); however, when comparing BRL-and spermine-induced NO increase in ventricular cardiomyocytes, BRL appears to lead also to robust NO generation (Figure 1f). Besides ventricular Figure 2 Immunohistochemical detection of activated eNOS (Bloch et al, 2001b) in the human right atrial (a-c, g-i) and left ventricular myocardium (d-f). A distinct increase in immunohistochemical detectable eNOS is visible in right atrial cardiomyocytes after BRL stimulation (b, c) compared to unstimulated right atrial cardiomyocytes (a).…”

Section: No Imagingmentioning

confidence: 99%

“…To investigate whether b 3 -adrenoceptor stimulation may influence eNOS activity in human myocardium, we performed immunohistochemical eNOS stainings in isolated, electrically stimulated right atrial and left ventricular nonfailing trabeculae under control conditions (t ¼ 0 min) and after application of BRL (10 mM, t ¼ 5 min), using an eNOS antibody which has been shown to specifically detect the activated, translocated eNOS protein (Bloch et al, 2001b). Figure 2 presents pictures taken from original immunostainings.…”

Section: Enos Activationmentioning

confidence: 99%

See 3 more Smart Citations

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Brixius

Bloch

Pott

et al. 2004

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

1 b-adrenoceptors are important modulators of cardiac function. The present study investigated b 3 -adrenergic eNOS activation in human myocardium. 2 We measured nitric oxide (NO) liberation (diaminofluorescence) and signal transduction (immunohistochemistry, phosphorylation of eNOS Ser1177 , eNOS Thr495 , eNOS Ser114 , Akt/protein kinase B (Akt/PKB), and eNOS translocation) in human right atrial (RA, aortocoronary-bypass OP) and left ventricular nonfailing (LV, rejected donor hearts) myocardium after application of BRL 37344 (BRL), a preferential b 3 -adrenoceptor agonist. 3 In both RA and LV, BRL (10 ml) induced a liberation of NO. An eNOS activation via translocation was only observed in RA after application of BRL (10 mM). Yet, the NO liberation in both LV and RA was accompanied by phosphorylation of eNOS Ser1177 and Akt/PKB. BRL-induced eNOS phosphorylation was abolished by LY292004, a blocker of PI-3 kinase. eNOS-Ser 114 phosphorylation was unchanged in RA, but decreased in LV after b 3 -adrenergic stimulation. BRL did not alter phosphorylation of eNOS Thr495 . 4 In conclusion, receptor-dependent eNOS activation is differentially regulated in the human heart. In the left ventricle, eNOS activation via phosphorylation seems to be of major importance, whereas in human atrial myocardium eNOS translocation is the predominant mechanism induced by b 3 -adrenergic activation.

show abstract

Section: Discussionmentioning

confidence: 87%

Section: Methodsmentioning

confidence: 99%

Section: No Imagingmentioning

confidence: 99%

Section: Enos Activationmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Brixius

Bloch

Pott

et al. 2004

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In ischemia myocardium, ischemia acts as a stimulus for eNOS activation resulting in increased eNOS activity and increased NO release. 51) We also checked the eNOS expression and found that eNOS expression was induced by puerarin in ischemic myocardium and non-ischemic myocardium of the rats with or without an increase of HIF-1a expression. We hypothesized that angiogenic effect of puerarin may attribute to inducing VEGF and/or eNOS expression.…”

Section: Discussionmentioning

confidence: 99%

Puerarin Induces Angiogenesis in Myocardium of Rat with Myocardial Infarction

Zhang

Chen

Yingjun

et al. 2006

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Puerarin is a major effective ingredient extracted from the traditional Chinese medicine Ge-gen (Radix Puerariae, RP). Recently, puerarin has been used to treat patients with coronary artery diseases (CAD). However, the mechanisms of puerarin on coronary artery diseases are still not very clear. In this study, we investigated the role of puerarin on angiogenesis in the non-ischemic and ischemic myocardium. We found that puerarin (120, 60 mg/kg, i.p.) could reduce infarct area in the heart of rat with myocardial infarction (MI). Puerarin (120 mg/kg) induced angiogenesis in the non-ischemic and ischemic myocardium, which was one of the mechanisms of curing coronary artery diseases. The gene expression or activation of vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1a a (HIF-1a a) and endothelial nitric oxide synthase (eNOS) that correlated with angiogenesis were also induced by puerarin. From these results, we suggested that puerarin may induce therapeutic angiogenesis in myocardium of rat with MI. The mechanism may be that puerarin can induce VEGF and eNOS expression.Key words angiogenesis; puerarin; myocardial infarction; vascular endothelial growth factor (VEGF); endothelial nitric oxide synthase (eNOS); hypoxia-inducible factor 1a (HIF-1a)

show abstract

β‐amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Misiti

Carelli-Alinovi

Sampaolese³

et al. 2012

Cell Biochemistry & Function

View full text Add to dashboard Cite

Until few years ago, many studies of Alzheimer's disease investigated the effects of this syndrome in the central nervous system. Only recently, the detection of amyloid beta peptide (Aβ) in the blood has evidenced the necessity to extend studies on extraneuronal cells, particularly on erythrocytes. Aβ is also present in brain capillaries, where it interacts with the erythrocytes, inducing several metabolic and functional alterations. Recently, functionally active endothelial type nitric oxide synthase (eNOS) was discovered in human erythrocytes. The goal of the present study was to evidence the effect of Aβ on erythrocyte eNOS. We found that Aβ following to 24-h exposure causes a decrease in the immune staining of erythrocyte eNOS. Concurrently, Aβ alters erythrocyte cell morphology, decreases nitrites and nitrates levels, and affects membrane acetylcholinesterase activity. Propidium, an acetylcholinesterase inhibitor, was able to reverse the effects elicited by Aβ. These events could contribute to the vascular alterations associated with Alzheimer's disease disease.

show abstract

Ischemia Increases Detectable Endothelial Nitric Oxide Synthase in Rat and Human Myocardium

Cited by 58 publications

References 38 publications

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Puerarin Induces Angiogenesis in Myocardium of Rat with Myocardial Infarction

β‐amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Contact Info

Product

Resources

About

Ischemia Increases Detectable Endothelial Nitric Oxide Synthase in Rat and Human Myocardium

Cited by 58 publications

References 38 publications

Mechanisms of β3‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Mechanisms of β3‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Puerarin Induces Angiogenesis in Myocardium of Rat with Myocardial Infarction

β‐amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Contact Info

Product

Resources

About

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium

Mechanisms of β₃‐adrenoceptor‐induced eNOS activation in right atrial and left ventricular human myocardium