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hypotension/tyrosine
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Effects of hemorrhagic hypotension on tyrosine concentrations in rat spinal cord and plasma.
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Tyrosine is the precursor for catecholamine neurotransmitters. When catecholamine-containing neurons are physiologically active (as sympathoadrenal cells are in hypotension), tyrosine administration increases catecholamine synthesis and release. Since hypotension can alter plasma amino acid
Tyrosine hydroxylase phosphorylation in catecholaminergic brain regions: a marker of activation following acute hypotension and glucoprivation.
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The expression of c-Fos defines brain regions activated by the stressors hypotension and glucoprivation however, whether this identifies all brain sites involved is unknown. Furthermore, the neurochemicals that delineate these regions, or are utilized in them when responding to these stressors
Decrease in the reactivity of locus coeruleus neurons to hypotension after an increase in their tyrosine hydroxylase content: a subregional in vivo voltammetry study in the rat.
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The aim of the present work was to determine if noradrenergic neurons of the anterior and the posterior subregions of the locus coeruleus exhibit a difference in reactivity in response to sodium nitroprusside-induced arterial hypotension, and if the pharmacological induction of tyrosine hydroxylase
Neurotensin Analogues Containing Cyclic Surrogates of Tyrosine at Position 11 Improve NTS2 Selectivity Leading to Analgesia without Hypotension and Hypothermia.
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Neurotensin (NT) exerts its analgesic effects through activation of the G protein-coupled receptors NTS1 and NTS2. This opioid-independent antinociception represents a potential alternative for pain management. While activation of NTS1 also induces a drop in blood pressure and body temperature, NTS2
pSer40 tyrosine hydroxylase immunohistochemistry identifies the anatomical location of C1 neurons in rat RVLM that are activated by hypotension.
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Identification of neurons, and their phenotype, that are activated in response to specific stimuli is a critical step in understanding how neural networks integrate inputs to produce specific outputs. Here, we developed novel mouse monoclonal antibodies of different IgG isotypes that are specific to
Effects of nitroprusside-induced hypotension on sympathetic nerve activity, tyrosine hydroxylase activity and [3H]norepinephrine uptake in rabbit vascular tissues.
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Catecholamines in turkeys with high or low blood pressure: effects of tyrosine hydroxylase inhibitor and ganglionic blocker.
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[Antagonism of L-tyrosine on progressive drop of the arterial pressure (tachyphylaxis) during adrenaline perfusion and on secondary hypotension caused by the interruption of the perfusion. Research of the mechanism of action].
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Hypotension and adrenal tyrosine hydroxylase in spontaneously hypertensive rats.
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Alpha 2-adrenergic receptor sensitivity in depressed patients: relation between 3H-yohimbine binding to platelet membranes and clonidine-induced hypotension.
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Alpha 2-adrenergic receptor changes during antidepressant treatment were studied using 3H-yohimbine binding to human platelet membranes and clonidine-induced hypotension. Twenty-six patients with major depressive disorder (MDD) participated for 4-6 weeks in a trial of imipramine (2.5 mg/kg/day),
Hypotension-induced expression of the c-fos gene in the medulla oblongata of piglets.
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Neural networks that mediate the reflex response to baroreceptor withdrawal were explored in Sus scrofa. Induction of c-fos was used as a monitor of synaptic activity in response to hypotension sustained by systemic administration of a peripheral vasodilator, sodium nitroprusside. Patterns of c-fos
Retrospective analysis of the safety and efficacy of high-dose interleukin-2 after prior tyrosine kinase inhibitor therapy in patients with advanced renal cell carcinoma.
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Although tyrosine kinase inhibitors (TKI) are the most common first-line therapy for metastatic renal cell carcinoma, high-dose interleukin-2 (HD-IL2) remains the only agent that provides durable complete responses. The optimal sequence of these agents remains uncertain. This retrospective
Intracranial hypotension with parkinsonism, ataxia, and bulbar weakness.
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OBJECTIVE
To describe a case of spontaneous intracranial hypotension with a previously unreported constellation of presenting features.
METHODS
Case report.
METHODS
Tertiary care center.
RESULTS
We describe a patient with intracranial hypotension who presented with a parkinsonian syndrome and later
NF-κB activation mediates LPS- or zymosan-induced hypotension and inflammation reversed by BAY61-3606, a selective Syk inhibitor, in rat models of septic and non-septic shock.
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We have previously demonstrated that the activation of the spleen tyrosine kinase (Syk)/inhibitory-κB (IκB)-α/nuclear factor-κB (NF-κB) p65 signalling pathway contributes to hypotension and inflammatory response in a rat models of zymosan (ZYM)-induced non-septic shock. The purpose of this study was
Clonidine and rilmenidine suppress hypotension-induced Fos expression in the lower brainstem of the conscious rabbit.
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Our current knowledge of the sites of action of the centrally-acting antihypertensive drug clonidine is based almost entirely on experiments in anesthetized animals. The aim of this study was to determine, in conscious rabbits, the sites of action in the brainstem of systemically administered
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