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Norepinephrine

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10581. Alphaxalone, a neurosteroid anesthetic, inhibits norepinephrine transporter function in cultured bovine adrenal medullary cells. (Abstract)

Alphaxalone, a neurosteroid anesthetic, inhibits norepinephrine transporter function in cultured bovine adrenal medullary cells. We studied the effects of alphaxalone, a neurosteroid anesthetic, on norepinephrine transporter (NET) function in cultured bovine adrenal medullary cells and the effect of a bolus injection of alphaxalone on blood pressure and serum norepinephrine (NE) levels in anesthetized rats. Alphaxalone (10-100 micro M) inhibited the desipramine-sensitive uptake of [(3)H]-NE (...) the desipramine-sensitive uptake of [(3)H]-norepinephrine (NE) by interfering with desipramine binding in bovine adrenal medullary cells. A bolus IV administration of alphaxalone slightly and significantly increased the serum NE levels in anesthetized rats. These findings suggest that alphaxalone competitively inhibits NE transporter function probably in sympathetic neurons.

2002 Anesthesia and Analgesia

10582. General anesthetic actions on norepinephrine, dopamine, and gamma-aminobutyric acid transporters in stably transfected cells. (Abstract)

General anesthetic actions on norepinephrine, dopamine, and gamma-aminobutyric acid transporters in stably transfected cells. The effects of general anesthetics on neurotransmitter uptake by plasma membrane transporters are controversial. We analyzed the effects of representative volatile and IV general anesthetics on recombinant transporters for norepinephrine (human NET), dopamine (rat DAT), or gamma-aminobutyric acid (rat GAT-1) stably expressed in a porcine kidney cell line (LLC-PK(1 (...) transmission. Recombinant transporters for norepinephrine and dopamine were sensitive to certain volatile and IV anesthetics, whereas gamma-aminobutyric acid transporters were insensitive. These anesthetic- and neurotransmitter-specific effects may underlie some of the secondary effects of general anesthetics.

2002 Anesthesia and Analgesia

10583. Immunolesion of norepinephrine and epinephrine afferents to medial hypothalamus alters basal and 2-deoxy-D-glucose-induced neuropeptide Y and agouti gene-related protein messenger ribonucleic acid expression in the arcuate nucleus. Full Text available with Trip Pro

Immunolesion of norepinephrine and epinephrine afferents to medial hypothalamus alters basal and 2-deoxy-D-glucose-induced neuropeptide Y and agouti gene-related protein messenger ribonucleic acid expression in the arcuate nucleus. Neuropeptide Y (NPY) and agouti gene-related protein (AGRP) are orexigenic peptides of special importance for control of food intake. In situ hybridization studies have shown that NPY and AGRP mRNAs are increased in the arcuate nucleus of the hypothalamus (ARC (...) ) by glucoprivation. Other work has shown that glucoprivation stimulates food intake by activation of hindbrain glucoreceptor cells and requires the participation of rostrally projecting norepinephrine (NE) or epinephrine (E) neurons. Here we determine the role of hindbrain catecholamine afferents in glucoprivation-induced increase in ARC NPY and AGRP gene expression. The selective NE/E immunotoxin saporin-conjugated antidopamine-beta-hydroxylase (anti-dbetah) was microinjected into the medial hypothalamus

2003 Endocrinology

10584. Expression of estrogen receptor-alpha and cFos in norepinephrine and epinephrine neurons of young and middle-aged rats during the steroid-induced luteinizing hormone surge. Full Text available with Trip Pro

Expression of estrogen receptor-alpha and cFos in norepinephrine and epinephrine neurons of young and middle-aged rats during the steroid-induced luteinizing hormone surge. Norepinephrine (NE) and epinephrine are important stimulators of GnRH release during the preovulatory surge in female rats. Previous studies have shown that the catecholaminergic neurons are sensitive to estradiol and that NE release in the hypothalamus is decreased in middle-aged rats at the time when the estrous cycles

2002 Endocrinology

10585. Immunotoxin lesion of hypothalamically projecting norepinephrine and epinephrine neurons differentially affects circadian and stressor-stimulated corticosterone secretion. Full Text available with Trip Pro

Immunotoxin lesion of hypothalamically projecting norepinephrine and epinephrine neurons differentially affects circadian and stressor-stimulated corticosterone secretion. Hindbrain norepinephrine (NE) and epinephrine (E) neurons play a pivotal role in the central distribution of sensory signals derived from the internal environment. Their projections influence the various secretory patterns of the hypothalamo-pituitary-adrenal axis and are essential for feeding and adrenal medullary responses

2003 Endocrinology

10586. Norepinephrine and epinephrine-deficient mice are hyperinsulinemic and have lower blood glucose. Full Text available with Trip Pro

Norepinephrine and epinephrine-deficient mice are hyperinsulinemic and have lower blood glucose. Norepinephrine (NE) and epinephrine (Epi) help maintain normal blood glucose levels by stimulating glucagon release, glycogenolysis, and food consumption, and by inhibiting insulin release. The absence of NE and Epi in dopamine beta-hydroxylase-null (Dbh-/-) mice results in chronically low blood glucose levels, an impaired glucagon response to hypoglycemia, and elevated insulin levels. Nevertheless

2003 Endocrinology

10587. Angiotensin II AT(1) and AT(2) receptors contribute to maintain basal adrenomedullary norepinephrine synthesis and tyrosine hydroxylase transcription. Full Text available with Trip Pro

Angiotensin II AT(1) and AT(2) receptors contribute to maintain basal adrenomedullary norepinephrine synthesis and tyrosine hydroxylase transcription. Angiotensin II (Ang II) AT(1) receptors have been proposed to mediate the Ang II-dependent and the stress-stimulated adrenomedullary catecholamine synthesis and release. However, in this tissue, most of the Ang II receptors are of the AT(2) type. We asked the question whether AT(1) and AT(2) receptors regulate basal catecholamine synthesis. Long (...) -term AT(1) receptor blockade decreased adrenomedullary AT(1) receptor binding, AT(2) receptor binding and AT(2) receptor protein, rat tyrosine hydroxylase (TH) mRNA, norepinephrine (NE) content, Fos-related antigen 2 (Fra-2) protein, phosphorylated cAMP response element binding protein (pCREB), and ERK2. Long-term AT(2) receptor blockade decreased AT(2) receptor binding, TH mRNA, NE content and Fra-2 protein, although not affecting AT(1) receptor binding or receptor protein, pCREB or ERK2

2003 Endocrinology

10588. Norepinephrine release is reduced in cardiac tissue of Type 2 diabetic patients. Full Text available with Trip Pro

Norepinephrine release is reduced in cardiac tissue of Type 2 diabetic patients. The aim of this study was to assess whether cardiac catecholamine release is affected in patients with Type 2 diabetes mellitus.A trial tissue was obtained from 19 diabetic (Type 2) and 43 non-diabetic patients undergoing coronary surgery. Endogenous norepinephrine release was examined under baseline conditions as well as during electrical field stimulation (effective voltage 5 V, stimulation frequency 4 Hz, pulse (...) width 2 msec) by high performance liquid chromatography and electrochemical detection. Cardiac function and arterial blood pressure was assessed from coronary angiography.In atrial tissue from diabetic patients, stimulation-induced norepinephrine release was reduced by 25% compared with non-diabetic patients, while baseline norepinephrine release did not differ between both groups. Preoperative plasma glucose and haemoglobin A(1C) concentrations were increased in patients with diabetes, however

2003 Diabetologia

10589. Signal transduction and Ca2+ signaling in contractile regulation induced by crosstalk between endothelin-1 and norepinephrine in dog ventricular myocardium. Full Text available with Trip Pro

Signal transduction and Ca2+ signaling in contractile regulation induced by crosstalk between endothelin-1 and norepinephrine in dog ventricular myocardium. In certain cardiovascular disorders, such as congestive heart failure and ischemic heart disease, several endogenous regulators, including norepinephrine (NE) and endothelin-1 (ET-1), are released from various types of cell. Because plasma levels of these regulators are elevated, it seems likely that cardiac contraction might be regulated

2003 Circulation Research

10590. Regional norepinephrine spillover in response to angiotensin-converting enzyme inhibition in healthy subjects. (Abstract)

Regional norepinephrine spillover in response to angiotensin-converting enzyme inhibition in healthy subjects. Even though most previous studies have shown that central nervous angiotensin II causes sympatho-excitation, there are data suggesting that blockade of the renin-angiotensin system (RAS) could activate the renal sympathetic nerves. The aim of the present study was to investigate overall, cardiac and renal sympathetic nerve activity, before and after intravenous enalaprilat, in healthy (...) dose of enalaprilat, whereas renal norepinephrine spillover increased after both doses by 49 and 26% respectively (P < 0.05 for both). Cardiac and total body norepinephrine spillover remained unchanged after both doses of enalaprilat. Pulmonary capillary wedge pressure, which was measured in eight subjects after 2.5 mg enalaprilat, fell by 43% (P < 0.05).In the absence of, or after a minor, blood pressure fall, intravenous enalaprilat selectively activates the renal nerves in healthy subjects

2003 Journal of Hypertension

10591. Increased cardiac norepinephrine release in spontaneously hypertensive rats: role of presynaptic alpha-2A adrenoceptors. (Abstract)

Increased cardiac norepinephrine release in spontaneously hypertensive rats: role of presynaptic alpha-2A adrenoceptors. An increased sympathoadrenergic activation is thought to contribute to the maintenance of elevated blood pressure levels in hypertension. Therefore, the regulation of cardiac presynaptic sympathetic neurotransmission was investigated in spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY).Electrical field stimulation (1 min, 4 Hz) evoked a higher norepinephrine (NE

2003 Journal of Hypertension

10592. Exogenous angiotensin II does not facilitate norepinephrine release in the heart. (Abstract)

Exogenous angiotensin II does not facilitate norepinephrine release in the heart. Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations (...) in the myocardial interstitial fluid (NE(MIF)) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE(MIF) was measured in the left ventricular myocardium using the microdialysis technique. Local infusion of angiotensin II into the left anterior descending coronary artery (LAD) at consecutive rates of 0.05, 0.5, and 5 ng/kg per minute did not affect NE(MIF), LAD flow, left ventricular dP

2002 Hypertension

10593. Conservation of the cardiostimulant effects of (-)-norepinephrine across Ser49Gly and Gly389Arg beta(1)-adrenergic receptor polymorphisms in human right atrium in vitro. (Abstract)

Conservation of the cardiostimulant effects of (-)-norepinephrine across Ser49Gly and Gly389Arg beta(1)-adrenergic receptor polymorphisms in human right atrium in vitro. The goal of this study was to determine whether the cardiostimulant effects of the endogenous beta(1)-adrenergic receptor (AR) agonist, (-)-norepinephrine are modified by polymorphic (Serine49Glycine [Ser49Gly], Glycine389Arginine [Gly389Arg]) variants of beta(1)-ARs in the nonfailing adult human heart.Human heart beta(1)-ARs (...) perform a crucial role in mediating the cardiostimulant effects of (-)-norepinephrine. An understanding of the significance of Ser49Gly and Gly389Arg polymorphisms in the human heart is beginning to emerge, but not as yet in adult patients who have coronary artery disease (CAD).The potency and maximal effects of (-)-norepinephrine at beta(1)-ARs (in the presence of beta(2)-AR blockade with 50 nM ICI 118,551 [erythro-DL-1(7-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol]) for changes in contractile

2002 Journal of the American College of Cardiology

10594. Hypoxia, angiotensin-II, and norepinephrine mediated apoptosis is stimulus specific in canine failed cardiomyocytes: a role for p38 MAPK, Fas-L and cyclin D1. (Abstract)

Hypoxia, angiotensin-II, and norepinephrine mediated apoptosis is stimulus specific in canine failed cardiomyocytes: a role for p38 MAPK, Fas-L and cyclin D1. Apoptosis may contribute to the myocardial dysfunction associated with heart failure (HF). Activation of the p38 MAPK cascade can induce apoptosis in non-cardiac cells through increased expression of Fas-L, or through decreased expression of cyclin D(1).We tested the hypothesis that hypoxia (HX), angiotensin-II (A-II) and norepinephrine

2003 European Journal of Heart Failure

10595. Estrogen depletion increases blood pressure and hypothalamic norepinephrine in middle-aged spontaneously hypertensive rats. Full Text available with Trip Pro

Estrogen depletion increases blood pressure and hypothalamic norepinephrine in middle-aged spontaneously hypertensive rats. In male spontaneously hypertensive rats (SHR) a high NaCl diet increases arterial pressure via a reduction in anterior hypothalamic nucleus norepinephrine release. Young female SHR are relatively well protected from this NaCl-sensitive hypertension, but depletion of both endogenous and dietary estrogens greatly exacerbates NaCl-sensitive hypertension. This study tests (...) the hypothesis that estrogen also protects late middle-aged female SHR from NaCl-sensitive hypertension and that this effect is mediated by an estrogen-related effect on hypothalamic norepinephrine release. Ten-month-old female SHR were ovariectomized and placed on a phytoestrogen-free diet containing either basal or high NaCl. Each rat was implanted with a silastic tube containing 17beta estradiol or vehicle. Three months later, arterial pressure and hypothalamic norepinephrine metabolite levels (MOPEG

2003 Hypertension

10596. Serum uric acid and plasma norepinephrine concentrations predict subsequent weight gain and blood pressure elevation. Full Text available with Trip Pro

Serum uric acid and plasma norepinephrine concentrations predict subsequent weight gain and blood pressure elevation. It has been reported that hypertension and obesity often coexist with hyperuricemia. To clarify the relations between serum uric acid, plasma norepinephrine, and insulin or leptin levels in subjects with weight gain-induced blood pressure elevation, we conducted the present longitudinal study. In 433 young, nonobese, normotensive men, body mass index, blood pressure, and levels (...) of serum uric acid, fasting plasma norepinephrine, insulin, and leptin were measured every year for 5 years. Subjects were stratified by significant weight gain and/or blood pressure elevation (>10% in body mass index or mean blood pressure) for 5 years. At entry, blood pressure, uric acid, and norepinephrine values in subjects with blood pressure elevation were greater than in those without it, although body mass index, insulin, and leptin were similar. At entry, body mass index, blood pressure, uric

2003 Hypertension

10597. PKC-zeta mediates norepinephrine-induced phospholipase D activation and cell proliferation in VSMC. Full Text available with Trip Pro

PKC-zeta mediates norepinephrine-induced phospholipase D activation and cell proliferation in VSMC. Norepinephrine (NE) stimulates phospholipase D (PLD) activity and cell proliferation in vascular smooth muscle cells (VSMCs). The objective of this study was to determine the contribution of PKC-zeta to NE-induced PLD activation and cell proliferation in VSMCs. PLD activity was measured by the formation of [3H]phosphatidylethanol in VSMCs labeled with [3H]oleic acid and exposed to ethanol. A high

2003 Hypertension

10598. Significance of matrix metalloproteinases in norepinephrine-induced remodelling of rat hearts. (Abstract)

Significance of matrix metalloproteinases in norepinephrine-induced remodelling of rat hearts. Norepinephrine (NE) induced hypertrophy and remodelling of the extracellular matrix (ECM) in the left ventricle (LV) of the rat heart with resulting fibrosis. However, there was no increased collagen deposition in the right ventricle (RV). To test the hypothesis that lack of RV fibrosis is the result of elevated cleavage of collagens we inhibited the activity of matrix metalloproteinases (MMP

2003 Cardiovascular Research

10599. Tracheal epinephrine or norepinephrine preceded by beta blockade in a dog model. Can beta blockade bestow any benefits? (Abstract)

Tracheal epinephrine or norepinephrine preceded by beta blockade in a dog model. Can beta blockade bestow any benefits? Tracheal epinephrine (adrenaline) has been associated with two major deletorious side effects: increased heart rate (HR) and an initial decrease of blood pressure (BP). This prospective randomized animal study compared the haemodynamic responses to tracheally administered epinephrine or norepinephrine (nor adrenaline) alone versus each after pretreatment with propranolol (...) for ameliorating those two untoward effects associated with epinephrine administration. Five anaesthetized mongrel dogs underwent 25 experiments of tracheal epinephrine or norepinephrine (0.02 mg/kg diluted with normal saline to 5 ml total volume) with or without an I/V non-selective beta-blocker (propranolol 0.1 mg/kg) pretreatment, and served as their own controls. Tracheal epinephrine alone produced a rise in both diastolic and mean arterial BP and an increase of HR. Tracheal norepinephrine alone produced

2003 Resuscitation

10600. Clinical studies on norepinephrine metabolism: how to interpret the numbers. (Abstract)

Clinical studies on norepinephrine metabolism: how to interpret the numbers. Metabolism, synthesis rates, and pharmacokinetics of major metabolites of endogenous norepinephrine were investigated in 38 drug-free depressed patients receiving a low monoamine diet on a closed ward. In a group of 21 patients, plasma and cerebrospinal fluid (CSF) concentrations of 3-methoxy-4-hydroxyphenyl-glycol (MHPG) correlated positively, but not significantly. In two groups of eight patients each, effects

1986 Psychiatry research

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