Neuronal nitric oxide synthase (NOS1) regulates beta-adrenergic contraction and calcium handling in isolated murine ventricular myocytes

Neuronal nitric oxide synthase (NOS1) regulates beta-adrenergic contraction and calcium handling in isolated murine ventricular myocytes

Sonraí bibleagrafaíochta
Príomhchruthaitheoirí:	Zhang, Y, Sears, C, Ashley, E, Kim, Y, Casadei, B
Formáid:	Conference item
Foilsithe / Cruthaithe:	2003

Míreanna comhchosúla

Cardiac nitric oxide synthase 1 regulates basal and beta-adrenergic contractility in murine ventricular myocytes.
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A cardiac neuronal nitric oxide synthase isoform regulates contraction and calcium handling in murine ventricular myocytes
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A cardiac neuronal nitric oxide synthase isoform regulates contraction and calcium handling in murine ventricular myocytes
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Enhancement of beta adrenergic responsiveness in myocytes lacking nitric oxide synthase 1
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Nitric oxide synthase 1 (NOS1) regulates basal and beta-adrenergic left-ventricular contraction and relaxation in vivo
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Nitric oxide synthase 1 (NOS1) regulates basal and beta-adrenergic left ventricular contraction and relaxation in vivo
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nNOS V eNOS mediated regulation of beta adrenergic inotropic and lusitropic responses in left ventricular myocytes
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Cardiac neuronal nitric oxide synthase isoform regulates myocardial contraction and calcium handling.
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Electrophysiological and mechanical properties of ventricular myocytes isolated from wild-type mice and mice with disruption of the neuronal nitric oxide synthase gene
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A cardiac nitric oxide synthase 1 regulates contraction and calcium fluxes - a novel mechanism in the autocrine control of cardiac function
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Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure
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Does nitric oxide regulate the hyperpolarisation-activated inward current in ventricular myocytes from spontaneously hypertensive rats?
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Does nitric oxide regulate the hyperpolarisation-activated inward current in ventricular myocytes from spontaneously hypertensive rats?
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Myocardial NOS1 controls the lusitropic response to beta-adrenergic stimulation in vivo and in vitro
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Reduced phospholamban phosphorylation is associated with impaired relaxation in left ventricular myocytes from neuronal NO synthase-deficient mice.
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Superoxide production by left ventricular myocytes in control and hypertrophied hearts
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Endogenous nitric oxide formation in cardiac myocytes does not control respiration during β‐adrenergic stimulation
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Nitric oxide does not modulate the hyperpolarization-activated current, I(f), in ventricular myocytes from spontaneously hypertensive rats.
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Impairment of cholinergic signaling reduces atrial beta-adrenergic responsiveness by enhancing eNOS expression
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Effect of disruption of the nNOS gene on myocardial calcium current and contraction
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Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.
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