Endothelial nitric oxide synthase decreases β-adrenergic responsiveness via inhibition of the L-type Ca<sup>2+</sup> current

Wang, Honglan; Kohr, Mark J.; Wheeler, Debra G.; Ziolo, Mark T.

doi:10.1152/ajpheart.01249.2007

Cited by 73 publications

(104 citation statements)

References 54 publications

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“…Mice lacking NOS3 display a slower heart rate, and an increase in the transient inward current that has been coupled to aminoglycoside-induced ventricular ectopy and tachycardia (182). While NOS3 -/ -myocytes have normal resting action potential duration (APD) and LTCC current under basal condition, their response to ISO is altered, with longer APD and augmented I Ca associated with increases in early and delayed afterdepolarizations (243). The latter may be related to a loss-of-negative cGMP/PKG effects on the bsubunit of the LTCC (256).…”

Section: Nos and Arrhythmiamentioning

confidence: 99%

Nitric Oxide Synthases in Heart Failure

Carnicer

Crabtree

Sivakumaran

et al. 2013

Antioxidants & Redox Signaling

151

138

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Significance: The regulation of myocardial function by constitutive nitric oxide synthases (NOS) is important for the maintenance of myocardial Ca 2+ homeostasis, relaxation and distensibility, and protection from arrhythmia and abnormal stress stimuli. However, sustained insults such as diabetes, hypertension, hemodynamic overload, and atrial fibrillation lead to dysfunctional NOS activity with superoxide produced instead of NO and worse pathophysiology. Recent Advances: Major strides in understanding the role of normal and abnormal constitutive NOS in the heart have revealed molecular targets by which NO modulates myocyte function and morphology, the role and nature of posttranslational modifications of NOS, and factors controlling nitroso-redox balance. Localized and differential signaling from NOS1 (neuronal) versus NOS3 (endothelial) isoforms are being identified, as are methods to restore NOS function in heart disease. Critical Issues: Abnormal NOS signaling plays a key role in many cardiac disorders, while targeted modulation may potentially reverse this pathogenic source of oxidative stress. Future Directions: Improvements in the clinical translation of potent modulators of NOS function/dysfunction may ultimately provide a powerful new treatment for many hearts diseases that are fueled by nitroso-redox imbalance.

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Section: Nos and Arrhythmiamentioning

confidence: 99%

Nitric Oxide Synthases in Heart Failure

Carnicer

Crabtree

Sivakumaran

et al. 2013

Antioxidants & Redox Signaling

151

138

View full text Add to dashboard Cite

show abstract

“…39 Therefore, the high nNOS levels during the animals active period when sympathetic activity is highest and subject to surges, could act to reduce the incidence of arrhythmias during periods of high stress. It remains to be seen whether diurnal variation in nNOS signaling are also present in other species, including man.…”

Section: Diurnal Variation In ␤-Adrenergic Stimulation Influences Arrmentioning

confidence: 99%

Inotropic Response of Cardiac Ventricular Myocytes to β-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation

Collins

Rodrigo

2010

Circulation Research

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“…Although HA inhibited H295R cell proliferation by increasing InsPn levels without activating aldosterone production, it is possible that HA stimulates NOS enzyme activity (via Ca 2C ), blocking steroidogenesis as described previously for MA-10 LCs by us (Mondillo et al 2009) and has been observed in other steroidogenic systems (Ducsay & Myers 2011). Regarding this, it has been demonstrated that NOS can inhibit L-type calcium channels (Wang et al 2008), which are necessary for AII-mediated steroidogenesis. Supposing that HA induced NOS in H295R cells, the entry of calcium through the L-channels would be blocked, thus preventing aldosterone synthesis, without affecting the proliferation pathway.…”

Section: Discussionmentioning

confidence: 61%

Histamine inhibits adrenocortical cell proliferation but does not affect steroidogenesis

Pagotto

Pereyra

Monzón

et al. 2014

Journal of Endocrinology

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Histamine (HA) is a neurotransmitter synthesized in most mammalian tissues exclusively by histidine decarboxylase enzyme. Among the plethora of actions mediated by HA, the modulatory effects on steroidogenesis and proliferation in Leydig cells (LCs) have been described recently. To determine whether the effects on LCs reported could be extrapolated to all steroidogenic systems, in this study, we assessed the effect of this amine on adrenal proliferation and steroidogenesis, using two adrenocortical cell lines as experimental models, murine Y1 cells and human NCI-H295R cells. Even when steroidogenesis was not modified by HA in adrenocortical cells, the biogenic amine inhibited the proliferation of H295R cells. This action was mediated by the activation of HRH1 subtype and an increase in the production of inositol phosphates as second messengers, causing cell-cycle arrest in the G2/M phase. These results indicate a new role for HA in the proliferation of human adrenocortical cells that could contribute to a better understanding of tumor pathology as well as to the development of new therapeutic agents.

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Endothelial nitric oxide synthase decreases β-adrenergic responsiveness via inhibition of the L-type Ca²⁺ current

Abstract: Wang H, Kohr MJ, Wheeler DG, Ziolo MT. Endothelial nitric oxide synthase decreases ␤-adrenergic responsiveness via inhibition of the L-type Ca 2ϩ current.

Cited by 73 publications

References 54 publications

Nitric Oxide Synthases in Heart Failure

Nitric Oxide Synthases in Heart Failure

Inotropic Response of Cardiac Ventricular Myocytes to β-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation

Histamine inhibits adrenocortical cell proliferation but does not affect steroidogenesis

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Endothelial nitric oxide synthase decreases β-adrenergic responsiveness via inhibition of the L-type Ca2+ current

Abstract: Wang H, Kohr MJ, Wheeler DG, Ziolo MT. Endothelial nitric oxide synthase decreases ␤-adrenergic responsiveness via inhibition of the L-type Ca 2ϩ current.

Cited by 73 publications

References 54 publications

Nitric Oxide Synthases in Heart Failure

Nitric Oxide Synthases in Heart Failure

Inotropic Response of Cardiac Ventricular Myocytes to β-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation

Histamine inhibits adrenocortical cell proliferation but does not affect steroidogenesis

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Endothelial nitric oxide synthase decreases β-adrenergic responsiveness via inhibition of the L-type Ca²⁺ current