Localization of NOS-1 in the sarcolemma region of a subpopulation of atrial cardiomyocytes including myoendocrine cells and NOS-3 in vascular and endocardial endothelial cells of the rat heart

Miethke, Alexander; Feussner, Markus; Planitzer, Gerit; Richter, H.; Gutsmann, Martina; Gossrau, Reinhart

doi:10.1078/0065-1281-00692

Cited by 16 publications

(6 citation statements)

References 40 publications

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“…TRIM did not alter basal DAF‐2 fluorescence, suggesting that nNOS, regardless of localisation, does not participate significantly in the background DAF‐2 fluorescence signal and basal release of NO. This suggests that the basal NO signal originates from an eNOS‐dependent source such as plasmalemmal and T‐tubule caveolae and within coronary endothelium (Miethke et al 2003; Massion et al 2004) where the majority of cardiac eNOS is considered to be located. Left ventricular pressure was decreased during perfusion of TRIM but perfusion pressure was not.…”

Section: Discussionmentioning

confidence: 99%

Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulation

Brack

Patel

Mantravardi

et al. 2009

The Journal of Physiology

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Abnormal autonomic activity has been shown to be a strong prognostic indicator of mortality in patients with heart failure (Nolan et al. 1998) and those who have had a previous myocardial infarct (La Rovere et al. 1998). Depressed heart rate variability and baroreceptor sensitivity are surrogate markers of impaired vagal tone associated with mortality in these conditions in which most of the deaths are sudden and due to ventricular arrhythmias, especially ventricular fibrillation (VF). We have recently shown that electrical stimulation of the vagus nerve in the neck ) has a strong anti-arrhythmic effect in the rabbit ventricle against VF. These effects are blocked in the presence of a nitric oxide (NO) synthase inhibitor providing indirect evidence that NO is involved in this effect. The implication of NO in mediating vagal activity in the ventricle is novel although

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Section: Discussionmentioning

confidence: 99%

Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulation

Brack

Patel

Mantravardi

et al. 2009

The Journal of Physiology

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“…In the normal ferret heart, nNOS is detectable at low levels in both right and left ventricles, predominating in left ventricular endocardium and septum (47). In rat hearts, nNOS predominates in atria (280).…”

Section: A Expression and Compartmentation Of The Nos In The Heart Amentioning

confidence: 97%

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

391

328

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Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in cardiovascular biology explains its growing implication in mechanosensitive aspects of integrated physiology, such as the control of blood pressure variability or the modulation of cardiac remodeling in situations of hemodynamic overload.

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“…It is likely that the basal fluorescence signal could originate from a number of sources since NO synthases can be found in endothelial cells (Miethke et al, 2003), neurones and nerve fibres of cardiac ganglia (Sosunov et al, 1996;Sosunov et al, 1995) and subcellularly located within cardiac myocytes e.g. sarcoplasmic reticulum and mitochondria (Xu et , 1999;Kanai et al, 2001).…”

Section: Origins Of Basal No Signalmentioning

confidence: 99%

A novel method of measuring nitric-oxide-dependent fluorescence using 4,5-diaminofluorescein (DAF-2) in the isolated Langendorff-perfused rabbit heart

Patel

Brack

Coote

et al. 2008

Pflugers Arch - Eur J Physiol

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4,5-diaminofluorescein (DAF-2) has been used to measure nitric oxide (NO) activity from a variety of preparations. The aim of this study was to develop a method to assess changes in NO fluorescence using DAF-2 in isolated rabbit hearts (2.0-2.5kg:n=8). Hearts were perfused in constant flow Langendorff mode and instrumented to record aortic perfusion pressure, left ventricular pressure and left ventricular epicardial fluorescence using a bifurcated light guide at excitation wavelengths of 470±10nm, 480±10nm, 490±10nm and 500±10nm collected at 535nm. DAF-2 DA was loaded using a single bolus 150μl (1μmol) injection. Changes in NOdependent fluorescence were determined using the NO donor sodium nitroprusside Our data suggests that DAF-2 DA is a useful fluorescence indicator for measuring NO activity in isolated hearts.

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Localization of NOS-1 in the sarcolemma region of a subpopulation of atrial cardiomyocytes including myoendocrine cells and NOS-3 in vascular and endocardial endothelial cells of the rat heart

Cited by 16 publications

References 40 publications

Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulation

Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulation

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

A novel method of measuring nitric-oxide-dependent fluorescence using 4,5-diaminofluorescein (DAF-2) in the isolated Langendorff-perfused rabbit heart

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