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[PMID]:27923789
[Au] Autor:Harvey RE; Barnes JN; Hart EC; Nicholson WT; Joyner MJ; Casey DP
[Ad] Endereço:Mayo Clinic College of Medicine, Mayo Clinic, Rochester, Minnesota.
[Ti] Título:Influence of sympathetic nerve activity on aortic hemodynamics and pulse wave velocity in women.
[So] Source:Am J Physiol Heart Circ Physiol;312(2):H340-H346, 2017 Feb 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Central (aortic) blood pressure, arterial stiffness, and sympathetic nerve activity increase with age in women. However, it is unknown if the age-related increase in sympathetic activity influences aortic hemodynamics and carotid-femoral pulse wave velocity (cfPWV), an index of central aortic stiffness. The goal of this study was to determine if aortic hemodynamics and cfPWV are directly influenced by sympathetic nerve activity by measuring aortic hemodynamics, cfPWV, and muscle sympathetic nerve activity (MSNA) in women before and during autonomic ganglionic blockade with trimethaphan camsylate. We studied 12 young premenopausal (23 ± 4 yr) and 12 older postmenopausal (57 ± 3 yr) women. These women did not differ in body mass index or mean arterial pressure ( > 0.05 for both). At baseline, postmenopausal women had higher aortic pulse pressure, augmented pressure, augmentation index adjusted for a heart rate of 75 beats/min, wasted left ventricular pressure energy, and cfPWV than young women ( < 0.05). During ganglionic blockade, postmenopausal women had a greater decrease in these variables in comparison to young women ( < 0.05). Additionally, baseline MSNA was negatively correlated with the reductions in aortic pulse pressure, augmented pressure, and wasted left ventricular pressure energy during ganglionic blockade in postmenopausal women ( < 0.05) but not young women. Baseline MSNA was not correlated with the changes in augmentation index adjusted for a heart rate of 75 beats/min or cfPWV in either group ( > 0.05 for all). Our results suggest that some aortic hemodynamic parameters are influenced by sympathetic activity to a greater extent in older postmenopausal women than in young premenopausal women. Autonomic ganglionic blockade results in significant decreases in multiple aortic pulse wave characteristics (e.g., augmented pressure) and central pulse wave velocity in older postmenopausal women but not in young premenopausal women. Certain aortic pulse wave parameters are negatively influenced by sympathetic activity to a greater extent in older postmenopausal women.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Aorta/efeitos dos fármacos
Pressão Arterial/efeitos dos fármacos
Bloqueadores Ganglionares/farmacologia
Hemodinâmica/efeitos dos fármacos
Análise de Onda de Pulso
Sistema Nervoso Simpático/efeitos dos fármacos
Trimetafano/farmacologia
[Mh] Termos MeSH secundário: Adulto
Aorta/inervação
Aorta/fisiologia
Pressão Arterial/fisiologia
Feminino
Gânglios Autônomos
Frequência Cardíaca
Hemodinâmica/fisiologia
Seres Humanos
Infusões Intravenosas
Meia-Idade
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/inervação
Pós-Menopausa
Pré-Menopausa
Sistema Nervoso Simpático/fisiologia
Rigidez Vascular/fisiologia
Vasodilatadores/farmacologia
Função Ventricular Esquerda
Pressão Ventricular/efeitos dos fármacos
Pressão Ventricular/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ganglionic Blockers); 0 (Vasodilator Agents); 6G8X656T45 (Trimethaphan); 8W556014K9 (trimethaphan camsylate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00447.2016


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[PMID]:25757803
[Au] Autor:Jordan J; Shibao C; Biaggioni I
[Ad] Endereço:Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany, Jordan.Jens@mh-hannover.de.
[Ti] Título:Multiple system atrophy: using clinical pharmacology to reveal pathophysiology.
[So] Source:Clin Auton Res;25(1):53-9, 2015 Feb.
[Is] ISSN:1619-1560
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Despite similarities in their clinical presentation, patients with multiple system atrophy (MSA) have residual sympathetic tone and intact post-ganglionic noradrenergic fibers, whereas patients with pure autonomic failure (PAF) and Parkinson disease have efferent post-ganglionic autonomic denervation. These differences are apparent biochemically, as well as in neurophysiological testing, with near normal plasma norephrine in MSA but very low levels in PAF. These differences are also reflected in the response patients have to drugs that interact with the autonomic nervous system. For example, the ganglionic blocker trimethaphan reduces residual sympathetic tone and lowers blood pressure in MSA, but less so in PAF. Conversely, the α2-antagonist yohimbine produces a greater increase in blood pressure in MSA compared to PAF, although significant overlap exists. In normal subjects, the norepinephrine reuptake (NET) inhibitor atomoxetine has little effect on blood pressure because the peripheral effects of NET inhibition that result in noradrenergic vasoconstriction are counteracted by the increase in brain norepinephrine, which reduces sympathetic outflow (a clonidine-like effect). In patients with autonomic failure and intact peripheral noradrenergic fibers, only the peripheral vasoconstriction is apparent. This translates to a significant pressor effect of atomoxetine in MSA, but not in PAF patients. Thus, pharmacological probes can be used to understand the pathophysiology of the different forms of autonomic failure, assist in the diagnosis, and aid in the management of orthostatic hypotension.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/fisiopatologia
Tratamento Farmacológico/métodos
Tratamento Farmacológico/tendências
Atrofia de Múltiplos Sistemas/tratamento farmacológico
Atrofia de Múltiplos Sistemas/fisiopatologia
[Mh] Termos MeSH secundário: Cloridrato de Atomoxetina/farmacologia
Cloridrato de Atomoxetina/uso terapêutico
Sistema Nervoso Autônomo/efeitos dos fármacos
Clonidina/farmacologia
Clonidina/uso terapêutico
Diagnóstico Diferencial
Seres Humanos
Alcaloides de Indol/farmacologia
Alcaloides de Indol/uso terapêutico
Atrofia de Múltiplos Sistemas/diagnóstico
Doença de Parkinson/diagnóstico
Doença de Parkinson/tratamento farmacológico
Doença de Parkinson/fisiopatologia
Insuficiência Autonômica Pura/diagnóstico
Insuficiência Autonômica Pura/tratamento farmacológico
Insuficiência Autonômica Pura/fisiopatologia
Brometo de Piridostigmina/farmacologia
Brometo de Piridostigmina/uso terapêutico
Trimetafano/farmacologia
Trimetafano/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indole Alkaloids); 0 (yohimbane); 57WVB6I2W0 (Atomoxetine Hydrochloride); 6G8X656T45 (Trimethaphan); KVI301NA53 (Pyridostigmine Bromide); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150312
[St] Status:MEDLINE
[do] DOI:10.1007/s10286-015-0271-4


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[PMID]:25001269
[Au] Autor:Gamboa A; Okamoto LE; Arnold AC; Figueroa RA; Diedrich A; Raj SR; Paranjape SY; Farley G; Abumrad N; Biaggioni I
[Ad] Endereço:From the Division of Clinical Pharmacology, Departments of Medicine (A.G., L.E.O., A.C.A., R.A.F., A.D., S.R.R., S.Y.P., G.F., I.B.), Pharmacology (S.R.R., I.B.), Biomedical Engineering (A.D.), and Surgery (N.A.), Vanderbilt University, Nashville, TN.
[Ti] Título:Autonomic blockade improves insulin sensitivity in obese subjects.
[So] Source:Hypertension;64(4):867-74, 2014 Oct.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity is an important risk factor for the development of insulin resistance. Initial compensatory mechanisms include an increase in insulin levels, which are thought to induce sympathetic activation in an attempt to restore energy balance. We have previously shown, however, that sympathetic activity has no beneficial effect on resting energy expenditure in obesity. On the contrary, we hypothesize that sympathetic activation contributes to insulin resistance. To test this hypothesis, we determined insulin sensitivity using a standard hyperinsulinemic euglycemic clamp protocol in obese subjects randomly assigned in a crossover design 1 month apart to receive saline (intact day) or trimetaphan (4 mg/min IV, autonomic blocked day). Whole-body glucose uptake (MBW in mg/kg per minute) was used as index of maximal muscle glucose use. During autonomic blockade, we clamped blood pressure with a concomitant titrated intravenous infusion of the nitric oxide synthase inhibitor N-monomethyl-L-arginine. Of the 21 obese subjects (43±2 years; 35±2 kg/m(2) body mass index) studied, 14 were insulin resistant; they were more obese, had higher plasma glucose and insulin, and had higher muscle sympathetic nerve activity (23.3±1.5 versus 17.2±2.1 burst/min; P=0.03) when compared with insulin-sensitive subjects. Glucose use improved during autonomic blockade in insulin-resistant subjects (MBW 3.8±0.3 blocked versus 3.1±0.3 mg/kg per minute intact; P=0.025), with no effect in the insulin-sensitive group. These findings support the concept that sympathetic activation contributes to insulin resistance in obesity and may result in a feedback loop whereby the compensatory increase in insulin levels contributes to greater sympathetic activation.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/efeitos dos fármacos
Bloqueadores Ganglionares/farmacologia
Resistência à Insulina/fisiologia
Obesidade/fisiopatologia
Trimetafano/farmacologia
[Mh] Termos MeSH secundário: Adulto
Sistema Nervoso Autônomo/fisiopatologia
Glicemia/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Estudos Cross-Over
Inibidores Enzimáticos/farmacologia
Feminino
Técnica Clamp de Glucose/métodos
Seres Humanos
Insulina/administração & dosagem
Insulina/sangue
Masculino
Meia-Idade
Músculos/inervação
Óxido Nítrico Sintase/antagonistas & inibidores
Óxido Nítrico Sintase/metabolismo
Obesidade/sangue
ômega-N-Metilarginina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Enzyme Inhibitors); 0 (Ganglionic Blockers); 0 (Insulin); 27JT06E6GR (omega-N-Methylarginine); 6G8X656T45 (Trimethaphan); EC 1.14.13.39 (Nitric Oxide Synthase)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:161215
[Lr] Data última revisão:
161215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140709
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.114.03738


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[PMID]:24324040
[Au] Autor:Barnes JN; Hart EC; Curry TB; Nicholson WT; Eisenach JH; Wallin BG; Charkoudian N; Joyner MJ
[Ad] Endereço:Department of Anesthesiology, Mayo Clinic, 200 1st St SW, SMH, Joseph 4-184, Rochester, MN 55905. Barnes.Jill@mayo.edu.
[Ti] Título:Aging enhances autonomic support of blood pressure in women.
[So] Source:Hypertension;63(2):303-8, 2014 Feb.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The autonomic nervous system plays a central role in both acute and chronic blood pressure regulation in humans. The activity of the sympathetic branch of the autonomic nervous system is positively associated with peripheral resistance, an important determinant of mean arterial pressure in men. In contrast, there is no association between sympathetic nerve activity and peripheral resistance in women before menopause, yet a positive association after menopause. We hypothesized that autonomic support of blood pressure is higher after menopause in women. We examined the effect of ganglionic blockade on arterial blood pressure and how this relates to baseline muscle sympathetic nerve activity in 12 young (25±1 years) and 12 older postmenopausal (61±2 years) women. The women were studied before and during autonomic blockade using trimethaphan camsylate. At baseline, muscle sympathetic nerve activity burst frequency and burst incidence were higher in the older women (33±3 versus 15±1 bursts/min; 57±5 versus 25±2 bursts/100 heartbeats, respectively; P<0.05). Muscle sympathetic nerve activity bursts were abolished by trimethaphan within minutes. Older women had a greater decrease in mean arterial pressure (-29±2 versus -9±2 mm Hg; P<0.01) and total peripheral resistance (-10±1 versus -5±1 mm Hg/L per minute; P<0.01) during trimethaphan. Baseline muscle sympathetic nerve activity was associated with the decrease in mean arterial pressure during trimethaphan (r=-0.74; P<0.05). In summary, our results suggest that autonomic support of blood pressure is greater in older women compared with young women and that elevated sympathetic nerve activity in older women contributes importantly to the increased incidence of hypertension after menopause.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Pressão Sanguínea/fisiologia
Hipertensão/fisiopatologia
Sistema Nervoso Simpático/fisiologia
Resistência Vascular/fisiologia
[Mh] Termos MeSH secundário: Adulto
Pressão Sanguínea/efeitos dos fármacos
Artéria Braquial/inervação
Artéria Braquial/fisiologia
Feminino
Bloqueadores Ganglionares/administração & dosagem
Seres Humanos
Menopausa/fisiologia
Meia-Idade
Músculo Esquelético/inervação
Músculo Esquelético/fisiologia
Nervo Fibular/fisiologia
Sistema Nervoso Simpático/efeitos dos fármacos
Trimetafano/administração & dosagem
Resistência Vascular/efeitos dos fármacos
Vasodilatadores/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ganglionic Blockers); 0 (Vasodilator Agents); 6G8X656T45 (Trimethaphan); 8W556014K9 (trimethaphan camsylate)
[Em] Mês de entrada:1403
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131211
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.113.02393


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[PMID]:22287587
[Au] Autor:Gamboa A; Okamoto LE; Diedrich A; Choi L; Robertson D; Farley G; Paranjape S; Biaggioni I
[Ad] Endereço:Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA. alfredo.gamboa@vanderbilt.edu
[Ti] Título:Sympathetic activation and nitric oxide function in early hypertension.
[So] Source:Am J Physiol Heart Circ Physiol;302(7):H1438-43, 2012 Apr 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to determine if tonic restrain of blood pressure by nitric oxide (NO) is impaired early in the development of hypertension. Impaired NO function is thought to contribute to hypertension, but it is not clear if this is explained by direct effects of NO on vascular tone or indirect modulation of sympathetic activity. We determined the blood pressure effect of NO synthase inhibition with N(ω)-monomethyl-l-arginine (L-NMMA) during autonomic blockade with trimethaphan to eliminate baroreflex buffering and NO modulation of autonomic tone. In this setting, impaired NO modulation of vascular tone would be reflected as a blunted pressor response to L-NMMA. We enrolled a total of 66 subjects (39 ± 1.3 yr old, 30 females), 20 normotensives, 20 prehypertensives (blood pressure between 120/80 and 140/90 mmHg), 17 hypertensives, and 9 smokers (included as "positive" controls of impaired NO function). Trimethaphan normalized blood pressure in hypertensives, suggesting increased sympathetic tone contributing to hypertension. In contrast, L-NMMA produced similar increases in systolic blood pressure in normal, prehypertensive, and hypertensive subjects (31 ± 2, 32 ± 2, and 30 ± 3 mmHg, respectively), whereas the response of smokers was blunted (16 ± 5 mmHg, P = 0.012). Our results suggest that sympathetic activity plays a role in hypertension. NO tonically restrains blood pressure by ∼30 mmHg, but we found no evidence of impaired modulation by NO of vascular tone contributing to the early development of hypertension. If NO deficiency contributes to hypertension, it is likely to be through its modulation of the autonomic nervous system, which was excluded in this study.
[Mh] Termos MeSH primário: Hipertensão/fisiopatologia
Óxido Nítrico/fisiologia
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Envelhecimento/fisiologia
Barorreflexo/efeitos dos fármacos
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Inibidores Enzimáticos/farmacologia
Feminino
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Masculino
Meia-Idade
Tono Muscular/efeitos dos fármacos
Tono Muscular/fisiologia
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/fisiologia
Antagonistas Nicotínicos/farmacologia
Óxido Nítrico Sintase Tipo III/antagonistas & inibidores
Receptores Nicotínicos/efeitos dos fármacos
Fumar/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
Trimetafano/farmacologia
Adulto Jovem
ômega-N-Metilarginina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Nicotinic Antagonists); 0 (Receptors, Nicotinic); 27JT06E6GR (omega-N-Methylarginine); 31C4KY9ESH (Nitric Oxide); 6G8X656T45 (Trimethaphan); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120131
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.01020.2011


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[PMID]:21362343
[Au] Autor:Wang JW; Zhao YW; Hou CL; Ni WF; Rui BY; Guo SC; Zheng XY; Dai KR
[Ad] Endereço:Department of Orthopaedic Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Ninth People's Hospital, Shanghai 200011, China.
[Ti] Título:An experimental study of artificial murine bladder reflex arc established by abdominal reflex.
[So] Source:Chin Med J (Engl);124(3):413-8, 2011 Feb.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The neurogenic bladder dysfunction caused by spinal cord injury is difficult to treat clinically. The aim of this research was to establish an artificial bladder reflex arc in rats through abdominal reflex pathway above the level of spinal cord injury, reinnervate the neurogenic bladder and restore bladder micturition. METHODS: The outcome was achieved by intradural microanastomosis of the right T13 ventral root to S2 ventral root with autogenous nerve grafting, leaving the right T13 dorsal root intact. Long-term function of the reflex arc was assessed from nerve electrophysiological data and intravesical pressure tests during 8 months postoperation. Horseradish peroxidase (HRP) tracing was performed to observe the effectiveness of the artificial reflex. RESULTS: Single stimulus (3 mA, 0.3 ms pulses, 20 Hz, 5-second duration) on the right T13 dorsal root resulted in evoked action potentials, raised intravesical pressures and bladder smooth muscle, compound action potential recorded from the right vesical plexus before and after the spinal cord transaction injury between L5 and S4 segmental in 12 Sprague-Dawley rats. There were HRP labelled cells in T13 ventral horn on the experimental side and in the intermediolateral nucleus on both sides of the L6-S4 segments after HRP injection. There was no HRP labelled cell in T13 ventral horn on the control side. CONCLUSION: Using the surviving somatic reflex above the level of spinal cord injury to reconstruct the bladder autonomous reflex arc by intradural microanastomosis of ventral root with a segment of autologous nerve grafting is practical in rats and may have clinical applications for humans.
[Mh] Termos MeSH primário: Reflexo Abdominal/fisiologia
Bexiga Urinaria Neurogênica/fisiopatologia
[Mh] Termos MeSH secundário: Anastomose Cirúrgica
Animais
Atropina/farmacologia
Masculino
Modelos Teóricos
Ratos
Ratos Sprague-Dawley
Reflexo Abdominal/efeitos dos fármacos
Trimetafano/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
6G8X656T45 (Trimethaphan); 7C0697DR9I (Atropine)
[Em] Mês de entrada:1106
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110303
[St] Status:MEDLINE


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[PMID]:20519311
[Au] Autor:Hesse C; Schroeder DR; Nicholson WT; Hart EC; Curry TB; Penheiter AR; Turner ST; Joyner MJ; Eisenach JH
[Ad] Endereço:Department of Anaesthesiology, Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA.
[Ti] Título:beta2-Adrenoceptor gene variation and systemic vasodilatation during ganglionic blockade.
[So] Source:J Physiol;588(Pt 14):2669-78, 2010 Jul 15.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Regional infusions of beta(2)-adrenoceptor (ADRB2) agonist have generally shown that individuals homozygous for Gly16 produces greater vasodilatation than those homozygous for Arg16. Systemic infusions have shown an opposite effect on systemic vascular resistance (SVR), possibly confounded by baroreflexes or interactions between single nucleotide polymorphism (SNP) positions 16 and 27. We tested the hypothesis that ADRB2 gene variation would influence the SVR response to ADRB2 agonist terbutaline (Terb) during ganglionic blockade. Forty healthy young adults were recruited according to the double homozygous haplotypes: Arg16 + Gln27 (n = 13), the rare Gly16 + Gln27 (n = 6), and Gly16 + Glu27 (n = 21). Arterial pressure was measured by brachial arterial catheter, and cardiac output by acetylene breathing. Lymphocytes were sampled for ex vivo analysis of ADRB2 density and binding conformation. Following baroreflex ablation with trimethaphan (3-7 mg min(1)), continuous phenylephrine was titrated to restore blood pressure to baseline. Terb was infused i.v. at 33 and 67 ng kg(1) min(1) for 15 min/dose. There was partial evidence to suggest a main effect of haplotype on the change in SVR (P = 0.06). For SNP position 16, the highest dose of Terb produced lower SVR in Gly16 (mean +/- s.e.m.: 7.5 +/- 0.4) vs. Arg16 (8.9 +/- 0.7 units; P = 0.03). Lymphocyte ADRB2 binding conformation was similar but receptor density was greater in Gly16 vs. Arg16 (P = 0.05). We conclude that during ganglionic blockade, the SVR response to systemic ADRB2 agonist is suggestive of augmented ADRB2 function in Gly16 + Glu27 homozygotes, with greater influence from Gly16, providing further evidence that ADRB2 gene variation influences vasodilatation.
[Mh] Termos MeSH primário: Receptores Adrenérgicos beta 2/genética
Receptores Adrenérgicos beta 2/fisiologia
Resistência Vascular/genética
Resistência Vascular/fisiologia
Vasodilatação/genética
[Mh] Termos MeSH secundário: Adolescente
Agonistas de Receptores Adrenérgicos beta 2
Agonistas Adrenérgicos beta/farmacologia
Adulto
Bloqueio Nervoso Autônomo
Barorreflexo/efeitos dos fármacos
Barorreflexo/genética
Barorreflexo/fisiologia
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/genética
Pressão Sanguínea/fisiologia
Artéria Braquial/efeitos dos fármacos
Artéria Braquial/fisiologia
Débito Cardíaco/efeitos dos fármacos
Débito Cardíaco/genética
Débito Cardíaco/fisiologia
Feminino
Bloqueadores Ganglionares/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/genética
Frequência Cardíaca/fisiologia
Seres Humanos
Masculino
Fenilefrina/farmacologia
Polimorfismo de Nucleotídeo Único
Terbutalina/farmacologia
Trimetafano/farmacologia
Resistência Vascular/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); 0 (Adrenergic beta-Agonists); 0 (Ganglionic Blockers); 0 (Receptors, Adrenergic, beta-2); 1WS297W6MV (Phenylephrine); 6G8X656T45 (Trimethaphan); N8ONU3L3PG (Terbutaline)
[Em] Mês de entrada:1011
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100604
[St] Status:MEDLINE
[do] DOI:10.1113/jphysiol.2010.190058


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[PMID]:19403604
[Au] Autor:Mitchell DA; Lambert G; Secher NH; Raven PB; van Lieshout J; Esler MD
[Ad] Endereço:Human Neurotransmitter Laboratory, Baker Medical Research Institute, Prahran, Victoria, Australia. davidmitchell2000@hotmail.com
[Ti] Título:Jugular venous overflow of noradrenaline from the brain: a neurochemical indicator of cerebrovascular sympathetic nerve activity in humans.
[So] Source:J Physiol;587(Pt 11):2589-97, 2009 Jun 01.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A novel neurochemical method was applied for studying the activity of sympathetic nerves in the human cerebral vascular system. The aim was to investigate whether noradrenaline plasma kinetic measurements made with internal jugular venous sampling reflect cerebrovascular sympathetic activity. A database was assembled of fifty-six healthy subjects in whom total body noradrenaline spillover (indicative of whole body sympathetic nervous activity), brain noradrenaline spillover and brain lipophlic noradrenaline metabolite (3,4-dihydroxyphenolglycol (DHPG) and 3-methoxy-4-hydroxyphenylglycol (MHPG)) overflow rates were measured. These measurements were also made following ganglion blockade (trimethaphan, n = 6), central sympathetic inhibition (clonidine, n = 4) and neuronal noradrenaline uptake blockade (desipramine, n = 13) and in a group of patients (n = 9) with pure autonomic failure (PAF). The mean brain noradrenline spillover and brain noradrenaline metabolite overflow in healthy subjects were 12.5 +/- 1.8, and 186.4 +/- 25 ng min(-1), respectively, with unilateral jugular venous sampling for both. Total body noradrenaline spillover was 605.8 ng min(-1) +/- 34.4 ng min(-1). As expected, trimethaphan infusion lowered brain noradrenaline spillover (P = 0.03), but perhaps surprisingly increased jugular overflow of brain metabolites (P = 0.01). Suppression of sympathetic nervous outflow with clonidine lowered brain noradrenaline spillover (P = 0.004), without changing brain metabolite overflow (P = 0.3). Neuronal noradrenaline uptake block with desipramine lowered the transcranial plasma extraction of tritiated noradrenaline (P = 0.001). The PAF patients had 77% lower brain noradrenaline spillover than healthy recruits (P = 0.06), indicating that in them sympathetic nerve degeneration extended to the cerebral circulation, but metabolites overflow was similar to healthy subjects (P = 0.3). The invariable discordance between noradrenline spillover and noradrenaline metabolite overflow from the brain under these different circumstances indicates that the two measures arise from different sources, i.e. noradrenaline spillover originates from the cerebral vasculature outside the blood-brain barrier, and the noradrenaline metabolites originate primarily from brain noradrenergic neurons. We suggest that measurements of transcranial plasma noradrenaline spillover have utility as a method for assessing the sympathetic nerve activity of the cerebral vasculature.
[Mh] Termos MeSH primário: Artérias Cerebrais/inervação
Veias Cerebrais/inervação
Circulação Cerebrovascular
Veias Jugulares
Norepinefrina/sangue
Insuficiência Autonômica Pura/sangue
Sistema Nervoso Simpático/metabolismo
[Mh] Termos MeSH secundário: Inibidores da Captação Adrenérgica/farmacologia
Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Circulação Cerebrovascular/efeitos dos fármacos
Clonidina/farmacologia
Bases de Dados como Assunto
Desipramina/farmacologia
Feminino
Bloqueadores Ganglionares/farmacologia
Seres Humanos
Cinética
Masculino
Metoxi-Hidroxifenilglicol/análogos & derivados
Metoxi-Hidroxifenilglicol/sangue
Valor Preditivo dos Testes
Insuficiência Autonômica Pura/fisiopatologia
Valores de Referência
Sistema Nervoso Simpático/efeitos dos fármacos
Simpatolíticos/farmacologia
Trimetafano/farmacologia
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Biomarkers); 0 (Ganglionic Blockers); 0 (Sympatholytics); 534-82-7 (Methoxyhydroxyphenylglycol); 6G8X656T45 (Trimethaphan); CF5G2G268A (dihydroxyphenylethylene glycol); MN3L5RMN02 (Clonidine); TG537D343B (Desipramine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090501
[St] Status:MEDLINE
[do] DOI:10.1113/jphysiol.2008.167999


  9 / 739 MEDLINE  
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[PMID]:18768769
[Au] Autor:Li M; Dai X; Watts S; Kreulen D; Fink G
[Ad] Endereço:Dept. of Pharmacology and Toxicology, B440 Life Sciences, Michigan State Univ., East Lansing, MI 48824, USA.
[Ti] Título:Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension.
[So] Source:Am J Physiol Regul Integr Comp Physiol;295(5):R1546-54, 2008 Nov.
[Is] ISSN:0363-6119
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin (ET) type B receptors (ET(B)R) are expressed in multiple tissues and perform different functions depending on their location. ET(B)R mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ET(B)R in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.
[Mh] Termos MeSH primário: Gânglios Simpáticos/metabolismo
Hipertensão/induzido quimicamente
Hipertensão/metabolismo
Superóxidos/metabolismo
Sistema Nervoso Simpático/metabolismo
Vasoconstritores/toxicidade
Venenos de Víboras/toxicidade
[Mh] Termos MeSH secundário: Acridinas
Animais
Denervação
Etídio/análogos & derivados
Corantes Fluorescentes
Gânglios Simpáticos/fisiologia
Bloqueadores Ganglionares/farmacologia
Luminescência
Masculino
Tono Muscular/fisiologia
Músculo Liso Vascular/inervação
Músculo Liso Vascular/metabolismo
Norepinefrina/sangue
Ratos
Ratos Sprague-Dawley
Trimetafano/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acridines); 0 (Fluorescent Dyes); 0 (Ganglionic Blockers); 0 (Vasoconstrictor Agents); 0 (Viper Venoms); 0 (sarafotoxins s6); 104821-25-2 (dihydroethidium); 11062-77-4 (Superoxides); 2315-97-1 (10,10'-dimethyl-9,9'-biacridinium); 6G8X656T45 (Trimethaphan); EN464416SI (Ethidium); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:0901
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080905
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00783.2007


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[PMID]:17687267
[Au] Autor:Wilkins BW; Hesse C; Charkoudian N; Nicholson WT; Sviggum HP; Moyer TP; Joyner MJ; Eisenach JH
[Ad] Endereço:Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
[Ti] Título:Autonomic cardiovascular control during a novel pharmacologic alternative to ganglionic blockade.
[So] Source:Clin Pharmacol Ther;83(5):692-701, 2008 May.
[Is] ISSN:1532-6535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to compare ganglionic blockade with trimethaphan (TMP) and an alternative drug strategy using combined muscarinic antagonist (glycopyrrolate, GLY) and alpha-2 agonist (dexmedetomidine, DEX). Protocol 1: incremental phenylephrine was administered during control and combined GLY-DEX, or control and TMP on two control combined GLY and DEX or TMP infusion on two randomized days. Protocol 2: muscle sympathetic nerve activity (MSNA) and the baroreflex MSNA relationship was determined before and after GLY-DEX. Blood pressure was higher with GLY-DEX (99+/-3 mm Hg) and lower with TMP (78+/-3 mm Hg) relative to control (GLY-DEX: 90+/-2 mm Hg; TMP: 91+/-2 mm Hg; P<0.05). Incremental phenylephrine increased pressure during GLY-DEX (P<0.01 vs control) and TMP (P<0.01 vs control) to a similar degree. Both GLY-DEX and TMP infusion inhibited norepinephrine release (P<0.01 vs control). GLY-DEX inhibited baseline MSNA (P<0.05) and baroreflex changes in MSNA (P<0.01). We conclude that the GLY-DEX alternative drug strategy can be used as a reasonable alternative to pharmacologic ganglionic blockade to examine autonomic cardiovascular control.
[Mh] Termos MeSH primário: Sistema Cardiovascular/efeitos dos fármacos
Dexmedetomidina/administração & dosagem
Bloqueadores Ganglionares/administração & dosagem
Glicopirrolato/administração & dosagem
Trimetafano/administração & dosagem
[Mh] Termos MeSH secundário: Agonistas alfa-Adrenérgicos/administração & dosagem
Adulto
Bloqueio Nervoso Autônomo/métodos
Barorreflexo/efeitos dos fármacos
Barorreflexo/fisiologia
Débito Cardíaco/efeitos dos fármacos
Sistema Cardiovascular/inervação
Catecolaminas/metabolismo
Feminino
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Masculino
Antagonistas Muscarínicos/administração & dosagem
Fenilefrina/administração & dosagem
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic alpha-Agonists); 0 (Catecholamines); 0 (Ganglionic Blockers); 0 (Muscarinic Antagonists); 1WS297W6MV (Phenylephrine); 67VB76HONO (Dexmedetomidine); 6G8X656T45 (Trimethaphan); V92SO9WP2I (Glycopyrrolate)
[Em] Mês de entrada:0804
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:070810
[St] Status:MEDLINE



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