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  1 / 23336 MEDLINE  
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PMID:29447158
Author:Ahmad A; Sattar MA; Azam M; Khan SA; Bhatt O; Johns EJ
Address:School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia.
Title:Interaction between nitric oxide and renal α1-adrenoreceptors mediated vasoconstriction in rats with left ventricular hypertrophyin Wistar Kyoto rats.
Source:PLoS One; 13(2):e0189386, 2018.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:Left ventricular hypertrophy (LVH) is associated with decreased responsiveness of renal α1-adrenoreceptors subtypes to adrenergic agonists. Nitric oxide donors are known to have antihypertrophic effects however their impact on responsiveness of renal α1-adrenoreceptors subtypes is unknown. This study investigated the impact of nitric oxide (NO) and its potential interaction with the responsiveness of renal α1-adrenoreceptors subtypes to adrenergic stimulation in rats with left ventricular hypertrophy (LVH). This study also explored the impact of NO donor on CSE expression in normal and LVH kidney. LVH was induced using isoprenaline and caffeine in drinking water for 2 weeks while NO donor (L-arginine, 1.25g/Lin drinking water) was given for 5 weeks. Intrarenal noradrenaline, phenylephrine and methoxamine responses were determined in the absence and presence of selective α1-adrenoceptor antagonists, 5- methylurapidil (5-MeU), chloroethylclonidine (CeC) and BMY 7378. Renal cortical endothelial nitric oxide synthase mRNA was upregulated 7 fold while that of cystathione γ lyase was unaltered in the NO treated LVH rats (LVH-NO) group compared to LVH group. The responsiveness of renal α1A, α1B and α1D-adrenoceptors in the low dose and high dose phases of 5-MeU, CEC and BMY7378 to adrenergic agonists was increased along with cGMP in the kidney of LVH-NO group. These findings suggest that exogenous NO precursor up-regulated the renal eNOS/NO/cGMP pathway in LVH rats and resulted in augmented α1A, α1B and α1D adrenoreceptors responsiveness to the adrenergic agonists. There is a positive interaction between H2S and NO production in normal animals but this interaction appears absent in LVH animals.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Receptors, Adrenergic, alpha-1); 31C4KY9ESH (Nitric Oxide)


  2 / 23336 MEDLINE  
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PMID:29364918
Author:Chamorro V; Morales-Cano D; Milara J; Barreira B; Moreno L; Callejo M; Mondejar-Parreño G; Esquivel-Ruiz S; Cortijo J; Cogolludo Á; Barberá JA; Perez-Vizcaino F
Address:Departamento de Farmacología. Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Title:Riociguat versus sildenafil on hypoxic pulmonary vasoconstriction and ventilation/perfusion matching.
Source:PLoS One; 13(1):e0191239, 2018.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:INTRODUCTION: Current treatment with vasodilators for pulmonary hypertension associated with respiratory diseases is limited by their inhibitory effect on hypoxic pulmonary vasoconstriction (HPV) and uncoupling effects on ventilation-perfusion (V'/Q'). Hypoxia is also a well-known modulator of the nitric oxide (NO) pathway, and may therefore differentially affect the responses to phosphodiesterase 5 (PDE5) inhibitors and soluble guanylyl cyclase (sGC) stimulators. So far, the effects of the sGC stimulator riociguat on HPV have been poorly characterized. MATERIALS AND METHODS: Contraction was recorded in pulmonary arteries (PA) in a wire myograph. Anesthetized rats were catheterized to record PA pressure. Ventilation and perfusion were analyzed by micro-CT-SPECT images in rats with pulmonary fibrosis induced by bleomycin. RESULTS: The PDE5 inhibitor sildenafil and the sGC stimulator riociguat similarly inhibited HPV in vitro and in vivo. Riociguat was more effective as vasodilator in isolated rat and human PA than sildenafil. Riociguat was ≈3-fold more potent under hypoxic conditions and it markedly inhibited HPV in vivo at a dose that barely affected the thromboxane A2 (TXA2) mimetic U46619-induced pressor responses. Pulmonary fibrosis was associated with V'/Q' uncoupling and riociguat did not affect the V'/Q' ratio. CONCLUSION: PDE5 inhibitors and sGC stimulators show a different vasodilator profile. Riociguat was highly effective and potentiated by hypoxia in rat and human PA. In vivo, riociguat preferentially inhibited hypoxic than non-hypoxic vasoconstriction. However, it did not worsen V'/Q' coupling in a rat model of pulmonary fibrosis.
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Enzyme Activators); 0 (Phosphodiesterase 5 Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 0 (Vasodilator Agents); BW9B0ZE037 (Sildenafil Citrate); EC 4.6.1.2 (Soluble Guanylyl Cyclase); RU3FE2Y4XI (riociguat)


  3 / 23336 MEDLINE  
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PMID:28463231
Author:Gaskill CF; Carrier EJ; Kropski JA; Bloodworth NC; Menon S; Foronjy RF; Taketo MM; Hong CC; Austin ED; West JD; Means AL; Loyd JE; Merryman WD; Hemnes AR; De Langhe S; Blackwell TS; Klemm DJ; Majka SM
Address:Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine or Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee USA.
Title:Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction.
Source:J Clin Invest; 127(6):2262-2276, 2017 Jun 01.
ISSN:1558-8238
Country of publication:United States
Language:eng
Abstract:Pulmonary vascular disease is characterized by remodeling and loss of microvessels and is typically attributed to pathological responses in vascular endothelium or abnormal smooth muscle cell phenotypes. We have challenged this understanding by defining an adult pulmonary mesenchymal progenitor cell (MPC) that regulates both microvascular function and angiogenesis. The current understanding of adult MPCs and their roles in homeostasis versus disease has been limited by a lack of genetic markers with which to lineage label multipotent mesenchyme and trace the differentiation of these MPCs into vascular lineages. Here, we have shown that lineage-labeled lung MPCs expressing the ATP-binding cassette protein ABCG2 (ABCG2+) are pericyte progenitors that participate in microvascular homeostasis as well as adaptive angiogenesis. Activation of Wnt/ß-catenin signaling, either autonomously or downstream of decreased BMP receptor signaling, enhanced ABCG2+ MPC proliferation but suppressed MPC differentiation into a functional pericyte lineage. Thus, enhanced Wnt/ß-catenin signaling in ABCG2+ MPCs drives a phenotype of persistent microvascular dysfunction, abnormal angiogenesis, and subsequent exacerbation of bleomycin-induced fibrosis. ABCG2+ MPCs may, therefore, account in part for the aberrant microvessel function and remodeling that are associated with chronic lung diseases.
Publication type:JOURNAL ARTICLE
Name of substance:0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Abcg2 protein, mouse); EC 2.7.11.30 (Bmpr2 protein, mouse); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II)


  4 / 23336 MEDLINE  
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PMID:29203629
Author:Vranish JR; Holwerda SW; Young BE; Credeur DP; Patik JC; Barbosa TC; Keller DM; Fadel PJ
Address:From the Department of Kinesiology, University of Texas at Arlington (J.R.V., B.E.Y., J.C.P., T.C.B., D.M.K., P.J.F.); School of Kinesiology, University of Southern Mississippi, Hattiesburg (D.P.C.); and Department of Health and Human Physiology, University of Iowa, Iowa City (S.W.H.).
Title:Exaggerated Vasoconstriction to Spontaneous Bursts of Muscle Sympathetic Nerve Activity in Healthy Young Black Men.
Source:Hypertension; 71(1):192-198, 2018 01.
ISSN:1524-4563
Country of publication:United States
Language:eng
Abstract:Blacks have the highest prevalence of hypertension, putting them at greater risk of cardiovascular disease and death. Previous studies have reported that, relative to whites, healthy black men have augmented pressor responses to sympathoexcitatory stressors. Although important, these studies do not inform about the resting state and the influence of spontaneous changes in resting muscle sympathetic nerve activity (MSNA). Likewise, little is known about the transduction of MSNA into a vascular response at rest on a beat-to-beat basis. Accordingly, we tested the hypothesis that relative to whites, blacks would exhibit greater vasoconstriction and pressor responses following spontaneous bursts of MSNA. Mean arterial pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 minutes of supine rest in 35 young healthy men (17 blacks and 18 whites). Signal averaging was used to characterize changes in leg vascular conductance, total vascular conductance, and mean arterial pressure following spontaneous MSNA bursts. Blacks demonstrated significantly greater decreases in leg vascular conductance (blacks: -15.0±1.0%; whites: -11.5±1.2%; =0.042) and total vascular conductance (blacks: -8.6±0.9%; whites: -5.1±0.4%; =0.001) following MSNA bursts, which resulted in greater mean arterial pressure increases (blacks: +5.2±0.6 mm Hg; whites: +3.9±0.3 mm Hg; =0.04). These exaggerated responses in blacks compared with whites were present whether MSNA bursts occurred in isolation (singles) or in combination (multiples) and were graded with increases in burst height. Collectively, these findings suggest that healthy young black men exhibit augmented sympathetic vascular transduction at rest and provide novel insight into potential mechanism(s) by which this population may develop hypertension later in life.
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL


  5 / 23336 MEDLINE  
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PMID:29203627
Author:Schinzari F; Tesauro M; Veneziani A; Mores N; Di Daniele N; Cardillo C
Address:From the Policlinico A. Gemelli, Rome, Italy (F.S., A.V., N.M., C.C.); Department of Internal Medicine, University of Tor Vergata, Rome, Italy (M.T., N.D.D.); and Departments of Surgery (A.V.), Pharmacology (N.M.), and Internal Medicine (C.C.), Catholic University, Rome, Italy.
Title:Favorable Vascular Actions of Angiotensin-(1-7) in Human Obesity.
Source:Hypertension; 71(1):185-191, 2018 01.
ISSN:1524-4563
Country of publication:United States
Language:eng
Abstract:Obese patients have vascular dysfunction related to impaired insulin-stimulated vasodilation and increased endothelin-1-mediated vasoconstriction. In contrast to the harmful vascular actions of angiotensin (Ang) II, the angiotensin-converting enzyme 2 product Ang-(1-7) has shown to exert cardiovascular and metabolic benefits in experimental models through stimulation of the Mas receptor. We, therefore, examined the effects of exogenous Ang-(1-7) on vasodilator tone and endothelin-1-dependent vasoconstriction in obese patients. Intra-arterial infusion of Ang-(1-7) (10 nmol/min) resulted in significant increase in unstimulated forearm flow ( =0.03), an effect that was not affected by the Mas receptor antagonist A779 (10 nmol/min; >0.05). In the absence of hyperinsulinemia, however, forearm flow responses to graded doses of acetylcholine and sodium nitroprusside were not different during Ang-(1-7) administration compared with saline (both >0.05). During infusion of regular insulin (0.15 mU/kg per minute), by contrast, endothelium-dependent vasodilator response to acetylcholine was significantly enhanced by Ang-(1-7) ( =0.04 versus saline), whereas endothelium-independent response to sodium nitroprusside was not modified ( =0.91). Finally, Ang-(1-7) decreased the vasodilator response to endothelin A receptor blockade (BQ-123; 10 nmol/min) compared with saline (6±1% versus 93±17%; <0.001); nitric oxide inhibition by l- -monomethylarginine (4 µmol/min) during concurrent endothelin A antagonism resulted in similar vasoconstriction in the absence or presence of Ang-(1-7 Ang-(1-7) ( =0.69). Our findings indicate that in obese patients Ang-(1-7) has favorable effects not only to improve insulin-stimulated endothelium-dependent vasodilation but also to blunt endothelin-1-dependent vasoconstrictor tone. These findings provide support for targeting Ang-(1-7) to counteract the hemodynamic abnormalities of human obesity.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Endothelin-1); 0 (Insulin); 0 (Peptide Fragments); 0 (Receptor, Endothelin A); 0 (Vasoconstrictor Agents); 0 (Vasodilator Agents); 9041-90-1 (Angiotensin I); IJ3FUK8MOF (angiotensin I (1-7))


  6 / 23336 MEDLINE  
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PMID:29212523
Author:Maeda T
Address:Department of Human Science, Faculty of Design, Kyushu University, 4-9-1, Shiobaru, Minami-ku, Fukuoka, 815-8540, Japan. maeda@design.kyushu-u.ac.jp.
Title:Relationship between maximum oxygen uptake and peripheral vasoconstriction in a cold environment.
Source:J Physiol Anthropol; 36(1):42, 2017 Dec 06.
ISSN:1880-6805
Country of publication:England
Language:eng
Abstract:BACKGROUND: Various individual characteristics affect environmental adaptability of a human. The present study evaluates the relationship between physical fitness and peripheral vasoconstriction in a cold environment. METHODS: Seven healthy male students (aged 22.0 years) participated in this study. Cold exposure tests consisted of supine rest for 60 min at 28 °C followed by 90 min at 10 °C. Rectal and skin temperatures at seven sites, oxygen consumption, and the diameter of a finger vein were measured during the experiment. Metabolic heat production, skin heat conductance, and the rate of vasoconstriction were calculated. Individual maximum oxygen consumption, a direct index of aerobic fitness, was measured on the day following the cold exposure test. RESULTS: Decreases in temperature of the hand negatively correlated with the changes in rectal temperature. Maximum oxygen consumption and the rate of vasoconstriction are positively correlated. Furthermore, pairs of the following three factors are also significantly correlated: rate of metabolic heat production, skin heat conductance, and the rate of vasoconstriction. CONCLUSION: The results of this study suggested that the capacity for peripheral vasoconstriction can be improved by physical exercise. Furthermore, when exposed to a cold environment, fitter individuals could maintain metabolic heat production at the resting metabolic level of a thermoneutral condition, as they correspondingly lost less heat.
Publication type:JOURNAL ARTICLE


  7 / 23336 MEDLINE  
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PMID:28295256
Author:Komatsu S; Kitazawa T; Ikebe M
Address:Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, Texas.
Title:Visualization of stimulus-specific heterogeneous activation of individual vascular smooth muscle cells in aortic tissues.
Source:J Cell Physiol; 233(1):434-446, 2018 Jan.
ISSN:1097-4652
Country of publication:United States
Language:eng
Abstract:Intercellular communication among autonomic nerves, endothelial cells (ECs), and vascular smooth muscle cells (VSMCs) plays a central role in an uninterrupted regulation of blood flow through vascular contractile machinery. Impairment of this communication is linked to development of vascular diseases such as hypertension, cerebral/coronary vasospasms, aortic aneurism, and erectile dysfunction. Although the basic concept of the communication as a whole has been studied, the spatiotemporal correlation of ECs/VSMCs in tissues at the cellular level is unknown. Here, we show a unique VSMC response to ECs during contraction and relaxation of isolated aorta tissues through visualization of spatiotemporal activation patterns of smooth muscle myosin II. ECs in the intimal layer dictate the stimulus-specific heterogeneous activation pattern of myosin II in VSMCs within distinct medial layers. Myosin light chain (MLC) phosphorylation (active form of myosin II) gradually increases towards outer layers (approximately threefold higher MLC phosphorylation at the outermost layer than that of the innermost layer), presumably by release of an intercellular messenger, nitric oxide (NO). Our study also demonstrates that the MLC phosphorylation at the outermost layer in spontaneously hypertensive rats (SHR) during NO-induced relaxation is quite high and approximately 10-fold higher than that of its counterpart, the Wister-Kyoto rats (WKY), suggesting that the distinct pattern of myosin II activation within tissues is important for vascular protection against elevated blood pressure.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Biomarkers); 0 (Myosin Light Chains); 31C4KY9ESH (Nitric Oxide); EC 3.6.1.- (Myosin Type II)


  8 / 23336 MEDLINE  
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PMID:29229127
Author:Peng TC; Chang CY; Huang IT; Kao MC; Chang YY; Huang CJ
Address:Department of Anesthesiology, Taipei Tzu Chi Hospital, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan.
Title:Platonin mitigates vascular hyporeactivity of thoracic aorta in septic rats.
Source:J Surg Res; 221:190-195, 2018 Jan.
ISSN:1095-8673
Country of publication:United States
Language:eng
Abstract:BACKGROUND: Vascular hyporeactivity contributes to hemodynamic alterations and circulatory failure in severe sepsis. Among the identified mechanisms, inflammation and oxidative stress are the most crucial ones in mediating the development of vascular hyporeactivity induced by sepsis. Platonin, a photosensitive dye and an antioxidant, possesses potent antiinflammation effects. We elucidated whether platonin could mitigate vascular hyporeactivity of thoracic aorta in septic rats. MATERIAL AND METHODS: Adult male Sprague-Dawley rats were randomized to receive sham operation (Sham), Sham plus platonin (100 µg/kg), cecal ligation and puncture (CLP), or CLP plus platonin (10, 50, or 100 µg/kg) and designated as the Sham, P, CLP, CLP + P(10), CLP + P(50), and CLP + P(100) group, respectively (n = 6 in each group). After maintaining for 12 hours, surviving rats were euthanized and thoracic aorta was isolated and vascular reactivity of aortic rings was determined. RESULTS: Vascular reactivity induced by vasoconstrictors phenylephrine and angiotensin II of the Sham and the P groups (n = 6 in both groups) were similar, whereas vascular reactivity of the CLP group (n = 5) were significantly lower than those of the Sham group (both P < 0.001). Of note, vascular reactivity induced by phenylephrine and angiotensin II of the CLP + P(10) group (n = 5) and the CLP group were not significantly different. In contrast, vascular reactivity induced by phenylephrine and angiotensin II of the CLP + P(50) and the CLP + P(100) groups (n = 6 in both groups) were significantly higher than those of the CLP group (phenylephrine: P = 0.024 and 0.017; angiotensin II: P = 0.031 and 0.036). CONCLUSION: Platonin could mitigate vascular hyporeactivity of thoracic aorta in septic rats.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Thiazoles); 0X9JDS6MF1 (platonin); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); K7Q1JQR04M (Dinoprostone)


  9 / 23336 MEDLINE  
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PMID:29200863
Author:Calderón-Gerstein WS; López-Peña A; Macha-Ramírez R; Bruno-Huamán A; Espejo-Ramos R; Vílchez-Bravo S; Ramírez-Breña M; Damián-Mucha M; Matos-Mucha A
Address:Department of Medicine, National Hospital Ramiro Prialé Prialé, Essalud Junín, Huancayo, Junín, Peru.
Title:Endothelial dysfunction assessment by flow-mediated dilation in a high-altitude population.
Source:Vasc Health Risk Manag; 13:421-426, 2017.
ISSN:1178-2048
Country of publication:New Zealand
Language:eng
Abstract:Introduction: Endothelial function at high altitude has been measured only in populations that are genetically adapted to chronic hypoxia. The objective of this study was to evaluate endothelial dysfunction (ED) in a nongenetically adapted high-altitude population of the Andes mountains, in Huancayo, Peru (3,250 meters above sea level). Methods: Participants included 61 patients: 28 cases and 33 controls. The cases were subjects with hypertension, diabetes mellitus, obesity, or a history of stroke or coronary artery disease. Flow-mediated vasodilation (FMD) of the brachial artery was measured in the supine position, at noon, after 5 minutes of resting. The brachial artery was identified above the elbow. Its basal diameter was measured during diastole, and FMD was tested after 5 minutes of forearm ischemia. Intima-media complex in the right carotid artery was also determined. An increase in the artery's baseline diameter <10% indicated a positive test. Endothelium-independent vasodilation was evaluated with sublingual nitrate administration. The intima-media complex in the right carotid artery was also measured. Results: 100% of diabetics had ED; ED was also found in 68.8% of obese individuals, 55% of hypertensive patients, and 46.5% of controls. Age, height, body mass index, and waist diameter were higher in the cases as compared with the controls. A total of 57.9% (n=11) of the cases and 45.2% (n=19) of the controls presented ED. Patients without ED had a mean increase in brachial artery diameter of 23.16%, while in those with ED it was only 3.84%. Individuals with diabetes or hypertension had a greater thickness of the carotid artery intima media layer (1.092 versus 0.664 cm) ( =0.037). A positive test for ED was associated with a greater basal diameter of the brachial artery (4.66±0.62 versus 4.23±0.59 cm) ( =0.02). A total of 7 patients presented paradoxical response, developing posthyperemia vasoconstriction. Discussion: The proportion of ED was high among controls and among patients with risk factors. Controls showed better FMD profiles than subjects studied in Tibet and the Himalayas.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Nitrates); 0 (Vasodilator Agents)


  10 / 23336 MEDLINE  
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PMID:28459438
Author:Li Y; Lucas-Osma AM; Black S; Bandet MV; Stephens MJ; Vavrek R; Sanelli L; Fenrich KK; Di Narzo AF; Dracheva S; Winship IR; Fouad K; Bennett DJ
Address:Neuroscience and Mental Health Institute and Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Alberta, Canada.
Title:Pericytes impair capillary blood flow and motor function after chronic spinal cord injury.
Source:Nat Med; 23(6):733-741, 2017 Jun.
ISSN:1546-170X
Country of publication:United States
Language:eng
Abstract:Blood vessels in the central nervous system (CNS) are controlled by neuronal activity. For example, widespread vessel constriction (vessel tone) is induced by brainstem neurons that release the monoamines serotonin and noradrenaline, and local vessel dilation is induced by glutamatergic neuron activity. Here we examined how vessel tone adapts to the loss of neuron-derived monoamines after spinal cord injury (SCI) in rats. We find that, months after the imposition of SCI, the spinal cord below the site of injury is in a chronic state of hypoxia owing to paradoxical excess activity of monoamine receptors (5-HT ) on pericytes, despite the absence of monoamines. This monoamine-receptor activity causes pericytes to locally constrict capillaries, which reduces blood flow to ischemic levels. Receptor activation in the absence of monoamines results from the production of trace amines (such as tryptamine) by pericytes that ectopically express the enzyme aromatic L-amino acid decarboxylase (AADC), which synthesizes trace amines directly from dietary amino acids (such as tryptophan). Inhibition of monoamine receptors or of AADC, or even an increase in inhaled oxygen, produces substantial relief from hypoxia and improves motoneuron and locomotor function after SCI.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Biogenic Monoamines); 0 (RNA, Messenger); 0 (Receptor, Serotonin, 5-HT1B); 0 (Receptors, Adrenergic, alpha-2); 0 (Receptors, Serotonin, 5-HT1); 0 (Serotonin 5-HT1 Receptor Antagonists); 0 (Tryptamines); 333DO1RDJY (Serotonin); 422ZU9N5TV (tryptamine); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases); S88TT14065 (Oxygen); X4W3ENH1CV (Norepinephrine); X8ZC7V0OX3 (Tyramine)



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