Impairment of cholinergic signaling reduces atrial beta-adrenergic responsiveness by enhancing eNOS expression

Impairment of cholinergic signaling reduces atrial beta-adrenergic responsiveness by enhancing eNOS expression

Bibliografiske detaljer
Main Authors:	Zhang, Y, Danson, E, Sears, C, Edwards, A, Casadei, B, Paterson, D
Format:	Conference item
Udgivet:	2004

Lignende værker

Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.
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The negative inotropic effect of beta(3)-adrenergic receptor stimulation in nNOS(-/-) mice is restored by oxypurinol
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Reduced phospholamban phosphorylation is responsible for impaired myocardial relaxation in nNOS(-/-) mice
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Reduced phospholamban phosphorylation is responsible for impaired myocardial relaxation in nNOS(-/-) mice
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Expression of eNOS in kidneys from hypertensive patients
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Myricetin ameliorated ischemia/reperfusion-induced brain endothelial permeability by improvement of eNOS uncoupling and activation eNOS/NO
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eNOS in congenital to adult cardiovascular disease
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PKC-dependent phosphorylation of eNOS at T495 regulates eNOS coupling and endothelial barrier function in response to G+ -toxins.
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Stoichiometric relationships between endothelial tetrahydrobiopterin, endothelial NO synthase (eNOS) activity, and eNOS coupling in vivo: insights from transgenic mice with endothelial-targeted GTP cyclohydrolase 1 and eNOS overexpression.
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Effects of inhibition of eNOS and nNOS on forearm blood flow during reflex sympathetic activation at rest and during exercise
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Loss of cholinergic innervation differentially affects eNOS-mediated blood flow, drainage of Aβ and cerebral amyloid angiopathy in the cortex and hippocampus of adult mice
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Neural control of coronary artery blood flow by non‐adrenergic and non‐cholinergic mechanisms
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Tetrahydrobiopterin- and glutathionylation-dependent regulation of eNOS coupling: Relationships revealed by eNOS glutathionylation mutants in cells with tet-regulated GTP cyclohydrolase I expression
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