Relevant bibliographies by topics / Pharmacology, Norepinephrine

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Pharmacology, Norepinephrine'

Author: Grafiati
Published: 10 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "Pharmacology, Norepinephrine"

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Carcillo, Joseph A., and Christopher J. Hough. "Norepinephrine induces expression of c-fos mRNA through the α-adrenoceptor in rat aortic rings." Canadian Journal of Physiology and Pharmacology 73, no. 9 (September 1, 1995): 1281–85. http://dx.doi.org/10.1139/y95-180.

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We examined whether norepinephrine at pharmacologically relevant doses induces increased expression of c-fos mRNA in rat aortic rings, c-fos mRNA was expressed at norepinephrine concentrations known to cause minimum and maximum contraction of rat aorta in vitro. At the concentration known to cause maximum contraction, norepinephrine produced a marked and sustained increase of c-fos mRNA expression. Induction of c-fos was blocked completely by the α1-adrenergic antagonist prazosin, partially by the α2-adrenergic antagonist yohimbine, and not at all by the β-adrenergic antagonist propranolol. A prazosin inhibition curve showed that 1 nmol/L prazosin inhibited 10 μmol/L norepinephrine induced c-fos expression by 40%. At the pharmacologic dose known to cause maximum contraction, norepinephrine induces c-fos mRNA expression through the α-adrenoceptor in rat aortic rings.Key words: vascular smooth muscle contraction, rat aorta, norepinephrine, c-fos mRNA expression, adrenergic receptor, catecholamine.
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Mitchell, Heather A., and David Weinshenker. "Good night and good luck: Norepinephrine in sleep pharmacology." Biochemical Pharmacology 79, no. 6 (March 2010): 801–9. http://dx.doi.org/10.1016/j.bcp.2009.10.004.

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Forrest, Christopher R., Ning Xu, and Cho Y. Pang. "Evidence for nicotine-induced skin flap ischemic necrosis in the pig." Canadian Journal of Physiology and Pharmacology 72, no. 1 (January 1, 1994): 30–38. http://dx.doi.org/10.1139/y94-006.

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There is clinical and experimental evidence to indicate that cigarette smoking may increase the risk of skin ischemic necrosis in flap surgery but the pathogenic mechanism remains unclear. The objectives of this project were to investigate the potential deleterious effects and mechanism of action of nicotine, a major by-product of cigarette smoking, in skin flap surgery in the pig. It was observed that 4–5 weeks of intramuscular nicotine injections (4 mg/kg; twice daily) significantly (p < 0.05) decreased the skin flap capillary blood flow and the length and area of skin flap viability in the pig. This nicotine treatment also induced a 1.6-fold increase in skin flap tissue content of norepinephrine compared with the saline-treated control. The estimated mean wet skin tissue content of norepinephrine (5 × 10−7 M) was much higher than the circulating level of norepinephrine (1.8 × 10−9 M) in nicotine-treated pigs. This level of norepinephrine (5 ×10−7 M) was seen to induce a significant vasoconstrictor effect (75% increase over basal perfusion pressure) in isolated perfused pig skin flaps. It was also observed that the vasoconstrictor effect of norepinephrine was significantly (p < 0.05) enhanced in the presence of 10−4 M Nω-monomethyl-L-arginine or NG-nitro-L-arginine, an endothelium-derived relaxing factor – nitric oxide (EDRF/NO) synthesis inhibitor. This vasoconstrictor effect was further enhanced in the presence of NG-nitro-L-arginine and 10−5 M indomethacin, a cyclooxygenase inhibitor. Taken together, these observations indicate that 4–5 weeks of nicotine treatment significantly reduced the skin capillary blood flow and viability in skin flap surgery in the pig and this deleterious effect was likely to be mediated, at least in part, by locally released norepinephrine induced by nicotine treatment. Furthermore, norepinephrine also induced skin flap local release of EDRF/NO and a vasodilating prostanoid that in turn attenuated norepinephrine's vasoconstrictor effect in the skin vasculature. We speculate that skin vasculature with compromised endothelial cell function as a result of trauma or disease is more susceptible to the vasoconstrictor effect of norepinephrine released by nicotine.Key words: chronic nicotine, norepinephrine, skin vasoconstriction, flap surgery.
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Li, Peter P., David Sibony, and Jerry J. Warsh. "Pharmacologic characterization of cirazoline-activated inositol phospholipid hydrolysis in rat brain cortical slices." Canadian Journal of Physiology and Pharmacology 66, no. 11 (November 1, 1988): 1460–63. http://dx.doi.org/10.1139/y88-238.

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Interaction of cirazoline, an imidazoline derivative, with α1-adrenoceptor coupled inositol phospholipid hydrolysis was characterized in rat brain cortical slices. Norepinephrine, a full α1-agonist, and phenylephrine, a partial α1-agonist, on inositol phospholipid hydrolysis were included for comparison. Norepinephrine produced a fourfold stimulation of inositol phospholipid hydrolysis, whereas cirazoline and phenylephrine caused only submaximal responses (40–60%) when compared with norepinephrine. The stimulation of inositol phospholipid hydrolysis by cirazoline was completely blocked by the α1-adrenoceptor antagonist prazosin, but not by selective α2- or β-adrenoceptor antagonists. Furthermore, the norepinephrine dose–response curve was shifted to the right in the presence of cirazoline, without affecting the maximal response. These results suggest that cirazoline behaves as a partial agonist at brain α1-adrenoceptors linked to inositol phospholipid hydrolysis.
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Stahl, Stephen M., Meghan M. Grady, Chantal Moret, and Mike Briley. "SNRIs: The Pharmacology, Clinical Efficacy, and Tolerability in Comparison with Other Classes of Antidepressants." CNS Spectrums 10, no. 9 (September 2005): 732–47. http://dx.doi.org/10.1017/s1092852900019726.

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AbstractThe class of serotonin and norepinephrine reuptake inhibitors (SNRIs) now comprises three medications: venlafaxine, milnacipran, and duloxetine. These drugs block the reuptake of both serotonin (5-HT) and norepinephrine with differing selectivity. Whereas milnacipran blocks 5-HT and norepinephrine reuptake with equal affinity, duloxetine has a 10-fold selectivity for 5-HT and venlafaxine a 30-fold selectivity for 5-HT. All three SNRIs are efficacious in treating a variety of anxiety disorders. There is no evidence for major differences between SNRIs and SSRIs in their efficacy in treating anxiety disorders. In contrast to SSRIs, which are generally ineffective in treating chronic pain, all three SNRIs seem to be helpful in relieving chronic pain associated with and independent of depression. Tolerability of an SNRI at therapeutic doses varies within the class. Although no direct comparative data are available, venlafaxine seems to be the least well-tolerated, combining serotonergic adverse effects (nausea, sexual dysfunction, withdrawal problems) with a dose-dependent cardiovascular phenomenon, principally hypertension. Duloxetine and milnacipran appear better tolerated and essentially devoid of cardiovascular toxicity.
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Vadiei, Nina, Mitchell J. Daley, Manasa S. Murthy, and Carrie S. Shuman. "Impact of Norepinephrine Weight-Based Dosing Compared With Non–Weight-Based Dosing in Achieving Time to Goal Mean Arterial Pressure in Obese Patients With Septic Shock." Annals of Pharmacotherapy 51, no. 3 (November 25, 2016): 194–202. http://dx.doi.org/10.1177/1060028016682030.

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Background: Currently, a lack of standardization exists in norepinephrine dosing units, the first-line vasopressor for septic shock. Timely achievement of goal mean arterial pressure (MAP) is dependent on optimal vasopressor dosing. Objective: To determine if weight-based dosing (WBD) of norepinephrine leads to earlier time to goal MAP compared with non-WBD in obese patients with septic shock. Methods: This was a retrospective, multicenter cohort study. Patients had a body mass index (BMI) ≥30 kg/m2 and received norepinephrine for septic shock with either a non-WBD strategy (between December 2009 and January 2013) or WBD strategy (between January 2013 and December 2015). The primary outcome was time to goal MAP. Secondary outcomes were norepinephrine duration, dose requirements, and development of treatment-related complications. Results: A total of 287 patients were included (WBD 144; non-WBD 143). There was no difference in median time to goal MAP (WBD 58 minutes, interquartile range [IQR] = 16.8-118.5, vs non-WBD 60 minutes, IQR = 17.5-193.5; P = 0.28). However, there was a difference in median cumulative norepinephrine dose (WBD 12.6 mg, IQR = 4.9-45.9, vs non-WBD 10.5 mg, IQR = 3.9-25.6; P = 0.04) and time to norepinephrine discontinuation (WBD 33 hours, IQR = 15-69, vs non-WBD 27 hours, IQR = 12-51; P = 0.03). There was no difference in rates of atrial fibrillation (WBD 15.3% vs non-WBD 23.7%; P = 0.07) or mortality (WBD 23.6% vs non-WBD 23.1%; P = 0.92). Conclusion: WBD of norepinephrine does not achieve time to goal MAP earlier in obese patients with septic shock. However, WBD may lead to higher norepinephrine cumulative dose requirements and prolonged time until norepinephrine discontinuation.
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Tatsuno, Tohru, Terufumi Kato, Michiko Katsuyama, and Mitsutaka Nakamura. "Chronic effects of L-threo-dihydroxyphenylserine, a precursor of (-)-norepinephrine, in norepinephrine-deficient mice." Japanese Journal of Pharmacology 49 (1989): 302. http://dx.doi.org/10.1016/s0021-5198(19)56743-9.

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Dong, Erdan, Akito Yatani, Amy Mohan, and Chang-seng Liang. "Myocardial β-adrenoceptor down-regulation by norepinephrine is linked to reduced norepinephrine uptake activity." European Journal of Pharmacology 384, no. 1 (November 1999): 17–24. http://dx.doi.org/10.1016/s0014-2999(99)00652-4.

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Lang, Chim C., Abdul R. Rahman, David J. K. Balfour, and Allan D. Struthers. "The differential effects of circulating norepinephrine and neuronally released norepinephrine on sodium excretion in humans." Clinical Pharmacology and Therapeutics 54, no. 5 (November 1993): 514–22. http://dx.doi.org/10.1038/clpt.1993.183.

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Stein, C. M., R. Nelson, H. B. He, M. Wood, and A. J. J. Wood. "Effects of Epinephrine on Norepinephrine Release." Clinical Pharmacology & Therapeutics 59, no. 2 (February 1996): 139. http://dx.doi.org/10.1038/sj.clpt.1996.55.

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Dissertations / Theses on the topic "Pharmacology, Norepinephrine"

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Stockmeier, Craig A., and Gregory A. Ordway. "Interactions of Norepinephrine With Other Neurotransmitter Systems: Anatomical Basis and Pharmacology." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/8614.

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Introduction Norepinephrine-containing neurons clustered within the locus coeruleus (LC) provide most of the norepinephrine present within the central nervous system. These cells have tonic pacemaker activity and this activity is regulated by a variety of neurotransmitter inputs. The focus of this review is primarily on classical, non-neuropeptide, neurotransmitter input to the LC and the reciprocal projections of noradrenergic neurons to those classical neurotransmitter systems. Input to the LC from serotonin-, dopamine-, γ-aminobutyric acid (GABA)-, glutamate-, and acetylcholine-containing neurons are described. In addition, input from the neuropeptide, substance P, receives attention because of the interest in this neuropeptide in psychiatric disease. Special attention is given to reciprocal projections from the LC to the monoamine neurotransmitters dopamine and serotonin. See Chapter 1 for a detailed description of the anatomy of the LC. Noradrenergic circuitry: input to the LC Early tract-tracing studies suggested that the LC received widespread input from many sites in the brain. A combination of techniques, however, including discrete injections of a more sensitive tract-tracing compound, anterograde labeling studies, and single-pulse stimulation studies forced a reconsideration of brain areas with direct input to the LC. The major afferents to the LC are rostral medullary in origin, with cell bodies located in the nucleus paragigantocellularis (PGi, using excitatory amino acid neurotransmitters) and nucleus prepositus hypoglossi (PrH, using GABA). However, dense projections from many brain regions terminate in the pericoerulear area, an area heavily invested with dendrites from LC neurons, and in the PGi and PrH.
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Turcotte, Julie. "Assessment of the serotonin and norepinephrine reuptake blocking properties of duloxetine in healthy subjects." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31550.

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Animal studies have shown that duloxetine is a dual inhibitor of norepinephrine (NE) and serotonin (5-HT) reuptake. The aim of this study was to assess the effects of duloxetine on the 5-HT and NE reuptake processes in healthy human volunteers. Twenty-seven healthy young males were randomly assigned to one of four groups, receiving one of the following daily drug regimens: placebo, clomipramine (a potent 5-HT/NE reuptake blocker) 100 mg/day, duloxetine 20 mg/day, or duloxetine 60 mg/day. In order to assess the NE reuptake process, the pressor response to intravenous tyramine was measured. Determination of the whole blood 5-HT content was used to evaluate the 5-HT reuptake blockade. These measurements were performed at baseline and repeated after 7 and 14 days of drug intake. Both duloxetine, at doses of 20 to 60 mg/day, and clomipramine significantly interfered with the 5-HT reuptake process, as demonstrated by marked decreases in blood 5-HT concentrations. However, the same doses of duloxetine, unlike clomipramine, failed to impede the usual increase in blood pressure that follows a tyramine intravenous infusion, indicating that clomipramine, but not duloxetine, blocked the NE reuptake process. At doses tested in healthy volunteers, duloxetine acted as a selective 5-HT reuptake inhibitor, having no clear effect on the NE reuptake process
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Herman, Anna. "Alteration of Monoaminergic Neuronal Firing by Acute Administration of Cariprazine: An In Vivo Electrophysiological Study." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36713.

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Cariprazine is a novel dopamine (DA) and serotonin (5-HT) partial agonist with an in vitro receptor affinity profile that endows it with the potential to be used successfully in the treatment of both unipolar and bipolar disorders. The objective of this study was to determine whether in vitro findings with cariprazine lead to functional alterations of monoamine systems in the intact rat brain. In vivo electrophysiological recordings were carried out in male Sprague-Dawley rats under chloral hydrate anesthesia. Dorsal raphé nucleus (DRN), locus coeruleus (LC), and hippocampus cornu ammonis region 3 (CA3) pyramidal neurons were recorded and cariprazine was administered systemically by intravenous injection or locally through iontophoresis. In the DRN, cariprazine induced a complete inhibition of the firing of 5-HT neurons, which was fully reversed by the selective 5-HT1A antagonist WAY100.635. In the LC, the inhibitory effect of the preferential 5-HT2A agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) was reversed by cariprazine with an ED50 value of 67 µg/kg, i.v., and it did not block the inhibitory effect of the α2-adrenergic agonist clonidine. In the hippocampus, when cariprazine was administered by iontophoresis, it inhibited the firing of pyramidal neurons, but it did not dampen the suppressant effect of 5-HT. These results indicate that, in vivo, cariprazine acts as a 5-HT1A agonist in the DRN, as an antagonist on 5-HT2A receptors controlling the firing of NE neurons, and is a full agonist at 5-HT1A receptors located on pyramidal neurons of the hippocampus. The modulatory actions of cariprazine on the 5-HT and NE systems may contribute to its reported effectiveness in depressive episodes.
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PACHMERHIWALA, RASHIDA. "Relationships between MDMA induced increases in extracellular glucose, glycogenolysis in brain and hyperthermia." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204751566.

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O'Neill, Brian. "Anatomy and Pharmacology of Dopamine Transporter-Mediated Reward and Locomotor Responses to Psychostimulants." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1352859081.

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Wei, Hua. "Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494.

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Nilsson, Ulrika K. "Lysophosphatidic acid : Physiological effects and structure-activity relationships." Doctoral thesis, Linköping : Univ, 2002. http://www.ep.liu.se/diss/med/07/51/index.html.

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Harris, Alan C. Jr. "N-methyl 4-methyl amphetamine N-alkyl chain extension differentially affects ion flux at the human dopamine and norepinephrine transporters." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4440.

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Amphetamine (AMPH) and its derivatives embody a remarkable breadth of pharmacology. These molecules exert their effects, both therapeutic and pathological, at the human monoamine transporters, which tune synaptic dynamics by evacuating monoamine neuromodulators from the synapse subsequent to neuronal impulses. These transporters are electrogenic, and the transporter-mediated current can be correlated to a surrogate measure of the change in membrane voltage: Ca++ currents from co-transfected L-type Ca++ channels. The present work makes use of this assay, with which it is possible to derive pharmacodynamic metrics from both substrates and inhibitors. This work presents data on a heretofore-unstudied class of amphetamine analogs: the enantiomers of N-Me 4-Me AMPH and N-Et 4-Me AMPH. Remarkably, while both enantiomers of the N-Me version of this compound function as substrates at hDAT, both enantiomers of the N-Et version are inhibitors. This switch does not occur at hNET, where all enantiomers of both N-Me and N-Et 4-Me AMPH function as substrates. Further, (S)-N-Et 4-Me AMPH is a substrate at dDAT. EC50 and IC50 values for all drugs at both transporters are presented. I present the results of super-resolution microscopic co-localization studies on the plasmalemmal spatial relation of the human dopamine transporter and voltage gated calcium channel, L-type 1.2 (CaV1.2). I discuss future aims toward a unified understanding of the mechanisms of monoamine transporter function, with an emphasis on what amphetamine can illuminate in this regard.
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FARINI, VALENTINA. "NUTRITIONAL AND HORMONAL MODULATION OF HUMAN MELANOMA PROGRESSION." Doctoral thesis, 2013. http://hdl.handle.net/2158/806331.

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The tumoral microenvironment, also called “tumor reactive stroma”, is composed by several heterotypic cells like cancer-associated fibroblasts (CAFs), pro inflammatory cells, endothelial cells and perycites which stroma create a complex and continuative “cross-talk” made of direct cell-to-cell contacts and paracrine/exocrine signals (growth factors, cytokines, soluble factors) promoting tumor development through stimulation of cancer cells survival/proliferation, migration and metastatic ability. The mediators of chronic stress norepinephrine (NE) and epinephrine (E) exert stimulant effects on the invasion process of a number of neoplastic cells, and this effect seems to be due, at least in part, to the interaction with β-adrenoceptors (AR), which are expressed by various malignant tumours. In particular, the expression of β-AR has been studied in various human solid tumors, such as breast, colon, prostatic, ovary, nasopharyngeal and oral cancer, raising the possibility that such receptors could affect invasion and dissemination processes. My study aimed to evaluate the expression of β-AR and the influence of NE and E on the malignant behaviour of melanoma cell lines. Preliminary results assessed by immunohistochemistry on a series of human benign and malignant melanocytic lesions showed that both β1- and β2-AR were expressed in melanocytic tumors, according to neoplastic progression, being significantly more expressed in malignant than benign lesions, and, for β2-AR, significantly more present in atypical than common naevi. In vitro studies demonstrated that primary and metastatic cell lines expressed both β-AR types and were stimulated by NE and/or E to secrete higher amounts of IL-6, VEGF and IL-8, which contribute to melanoma progression, while NE enhanced motility through matrix metalloprotease-2. The pro-invasive effect of NE and E was inhibited by non-selective AR inhibitor propanolol, confirming β-AR involvement. In addition, VEGF increased the invasive spur induced by NE in A375 cell line, while IL-6 in association with NE could activate dermal fibroblasts toward a myofibroblastic phenotype, typical of tumour microenvironment. Taken together the results suggest that NE and E can dramatically affect the aggressiveness of melanoma cells and, since primary and metastatic melanomas exhibit strongly β-AR expression, could affect the course of the disease in melanoma patients too. These data support the hypothesis that the interaction of cathecolamines with β-AR could be a useful target in oncologic therapy in order to prevent melanoma metastatic progression. Beside and in synergy with signals produced by tumor micorenvironment, cancer cells are also able to completely modify their metabolic behaviour in order to sustain cancer progression. In particular, there is growing interest in defining the role of reactive stroma in the regulation of cancer cells metabolism. At this purpose, the “Warburg effect” is the best known tumor-specific alteration of common metabolic pathways, as cancer cells show increased glycolysis even in conditions of high oxygen tension (‘‘aerobic glycolysis’’), leading to high lactate production. In addition, cancer cells can use elevated amounts of glucose as a carbon source for anabolic reactions. The aim of the second part of my study is to focus on the ability of nutrients to regulate transcription factors involved in cancer cells metabolism. One of these factors is represented by hypoxia inducible factor-1α (HIF-1α). It is well established that, under hypoxic condition, HIF-1α activates target genes whose protein products mediate a switch from oxidative to glycolytic metabolism (ex. GLUT-1, LDH-A), while it is not well established yet the role of HIF-1α in regulating these complex pathways under normoxic condition. To this purpose, A375 primary melanoma cell line was cultured in normoxic condition in presence/absence of nutrients like glucose, pyruvate and lactate in order to understand how different nutrients can activate key pathways for cancer progression. Cytofluorimetric analysis demonstrate that A375 show strong dependance on glucose content of media in order to sustain survival, thereby according to a Warburg metabolic phenotype, and that nutrients alone are able to induce the expression of HIF-1α and of its target gene carbonic anidrase-IX (CA-IX), probably thorugh an increased reactive oxygen species (ROS) production. In order to further understand the role of nutrients-induced HIF-1α, we performed migration and invasion assays with Boyden chambers, respectively in absence or presence of Matrigel mimicking the extracellular matrix. Nutrients alone are also able to elicit a pro-invasive response of A375 and this effect is reverted after both treatment with Topotecan, a HIF-1α farmacological inhibitor, and HIF-1α gene silencing. Finally, data obtained so far allow us to hypothesize a novel important role of nutrients-induced HIF-1α normoxic stabilization in order to sustain cancer progression.
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Walsh, Kathryn. "Norepinephrine-evoked renal regulation of sodium homeostasis in salt-sensitive hypertension." Thesis, 2016. https://hdl.handle.net/2144/16730.

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Hypertension affects 1 in 3 adults and is the single greatest risk factor for premature death. Salt-sensitive hypertension occurs in approximately 50% of hypertensive patients and results in a 3-fold increase in the risk of adverse cardiovascular events. However, the pathophysiology of salt-sensitive hypertension remains to be fully elucidated. There has been increased interest in the interaction between the sympathetic nervous system and the kidney and how that interaction mediates sodium excretion to drive the development of salt-sensitivity. Previous studies show that sympathetic over-activity increases expression of the sodium chloride cotransporter (NCC) resulting in increased NCC-mediated sodium reabsorption, and the development of salt-sensitive hypertension. In this thesis, I show the effect of increased norepinephrine (NE) and high salt intake in salt-resistant vs. salt-sensitive rat phenotypes on blood pressure regulation, NCC activity, and the adrenoreceptor-mediated regulatory kinase network signal transduction pathway. A high salt diet 1) exacerbates NE-induced hypertension in salt-resistant Sprague-Dawley (SD) rats and 2) results in hypertension in Dahl salt-sensitive (DSS) rats. In contrast to salt-resistant phenotypes (SD & Dahl salt-resistant), dietary sodium-evoked suppression of NCC expression and activity is prevented in salt-sensitive rats (SD-NE infusion & DSS) - I show that this occurs through a failure of a high salt intake to suppress renal OxSR1, SPAK, and WNK1 (NCC regulatory proteins). I demonstrate that α1-adrenoreceptors are responsible for mediating the salt-sensitive component of hypertension and restore dietary sodium-evoked suppression of the NCC via a predominant OxSR1 pathway. Chronic β-adrenoreceptor antagonism significantly reduces blood pressure in NE-mediated hypertension. How the body senses salt remains unknown, but my data show that selective removal of the afferent renal nerves prevents dietary sodium-evoked suppression of NCC expression and activity resulting in salt-sensitive hypertension, suggesting that the afferent renal nerves play an important role as a sodium-sensing mechanism. Overall, these data demonstrate that attenuated afferent renal nerve feedback drives renal efferent nerve release of NE to prevent the downregulation of the NCC via an α1-adrenergic receptor-gated WNK1-OxSR1 signal transduction pathway to evoke the development of salt-sensitive hypertension.
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Books on the topic "Pharmacology, Norepinephrine"

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J, Heal David, and Marsden C. A, eds. The Pharmacology of noradrenaline in the central nervous system. Oxford [England]: Oxford University Press, 1990.

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ed, Vanhoutte Paul M., and International Symposium [on Return Circulation and Norepinephrine] (3rd : 1990 : Cairo, Egypt), eds. Return circulation and norepinephrine: An update : proceedings of the 3rd International Symposium held in Cairo (Egypt) March 12-17th, 1990. Paris: J. Libbey Eurotext, 1991.

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M, Vanhoutte Paul, ed. Return circulation and norepinephrine--an update: Proceedings of the 3rd International Symposium held in Cairo (Egypt) March 12-17th, 1990. Paris: John Libbey Eurotext, 1991.

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Return Circulation and Norepinephrine. John Libbey & Co Ltd, 1991.

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Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.

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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
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Book chapters on the topic "Pharmacology, Norepinephrine"

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Blier, P., and C. Montigny. "Antidepressant Monoamine Oxidase Inhibitors Enhance Serotonin but not Norepinephrine Neurotransmission." In Clinical Pharmacology in Psychiatry, 127–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71288-3_15.

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Bylund, David B. "Norepinephrine." In xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62303-7.

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Vaughan, Roxanne. "NET, Norepinephrine Transporter." In xPharm: The Comprehensive Pharmacology Reference, 1–11. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60443-x.

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Persico, Amelia L., Erica L. Wegrzyn, and Jeffrey Fudin. "Methadone and Levorphanol." In Pain, 151–56. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197542873.003.0018.

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Levorphanol and methadone share the unique pharmacology of potent, full mu-opioid receptor agonism combined with inhibition of the reuptake of norepinephrine and serotonin as well as NMDA receptor blockade. Of note, methadone is a more potent serotonin reuptake inhibitor than levorphanol, and serotonin does not contribute to its anti-nociceptive activity. In addition to their overlapping pharmacology, levorphanol is also a kappa opioid and delta opioid receptor agonist. Given their shared activity as mu opioid agonists, NMDA antagonists, and noradrenergic activity, both therapies reduce the perception of nociceptive and neuropathic pain; NMDA antagonism blocks the flood of glutamate associated with neuropathic pain from binding to NMDA receptors thus reducing neuropathic pain experience, and inhibiting the reuptake of norepinephrine leaves more norepinephrine available in neuronal synapses to bind alpha-2-adrenergic receptors. These unique properties make the use of levorphanol and methadone valuable in palliative care.
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Justice, J. B., K. S. Danek, J. W. Kable, E. L. Barker, and R. D. Blakely. "Voltammetric Approaches to Kinetics and Mechanism of the Norepinephrine Transporter." In Advances in Pharmacology, 191–94. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60725-5.

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Breier, Alan, Lgor Elman, and David S. Goldstein. "Norepinephrine and Schizophrenia: A New Hypothesis for Antipsychotic Drug Action." In Advances in Pharmacology, 785–88. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60864-9.

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Ainsworth, Sean. "N." In Neonatal Formulary, edited by Sean Ainsworth, 537–66. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198840787.003.0026.

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This chapter presents information on neonatal drugs that begin with N, including use, pharmacology, adverse effects, fetal and infant implications of maternal treatment, treatment, and supply of Naloxone, Neostigmine (and pyridostigmine), Nevirapine, Nifedipine, Nitazoxanide, Nitisinone, Nitric oxide, Nitrofurantoin, Nitrous oxide, Noradrenaline = Norepinephrine (rINN), and Nystatin
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Stjärne, Lennart. "Pattern of Adenosine Triphosphate and Norepinephrine Release and Clearance: Consequences for Neurotransmission." In Advances in Pharmacology, 114–19. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60709-7.

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Esler, M., G. Lambert, G. Jennings, A. Turner, and D. Kaye. "Central and Peripheral Norepinephrine Kinetics in Heart Failure, Coronary Artery Disease, and Hypertension." In Advances in Pharmacology, 650–53. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60835-2.

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Bönisch, H., R. Hammermann, and M. Brüss. "Role of Protein Kinase C and Second Messengers in Regulation of the Norepinephrine Transporter." In Advances in Pharmacology, 183–86. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60723-1.

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Conference papers on the topic "Pharmacology, Norepinephrine"

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Timokhina, Ekaterina Petrovna, Nataliya Valentinovna Yaglova, Sergey Stanislavovich Obernikhin, Valentin Vasilyevich Yaglov, Svetlana Vladimirovna Nazimova, and Dibakhan Aslanbekovna Tsomartova. "SENSITIVITY OF CATHEHOLAMINE-PRODUCING STRUCTURES TO DISRUPTIVE ACTION OF DDT." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.11.

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The results of the research revealed that norepinephrine-produsing formations demonstrate higher sensitivity to low-dose exposure to endocrine disrupting chemical DDT than epinephrine-producing ones. Differences in sensitivity to endocrine disruption remains unchanged whatever onset of exposure is prenatal or postnatal period of ontogeny.
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Journal articles
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