Search results for "Adrenergic"

showing 10 items of 433 documents

Differential blockade by nifedipine and ω-conotoxin GVIA of α1- and β1-adrenoceptor-controlled calcium channels on motor nerve terminals of the rat

1990

Electrically evoked release of [3H]acetylcholine ([3H]ACh) from the rat phrenic nerve and its facilitation by stimulation of presynaptic alpha 1- and beta 1-adrenoceptors were investigated in the absence and presence of nifedipine and omega-conotoxin GVIA. Both calcium channel antagonists did not modify electrically evoked [3H]ACh release, but selectively blocked the effect triggered by both facilitatory adrenergic receptors. The increase in [3H]ACh release mediated via beta 1-adrenoceptor activation was abolished by low concentrations (1 nM) of omega-conotoxin GVIA, whereas nifedipine (100 nM) abolished the facilitatory effect mediated via alpha 1-adrenoceptor stimulation. Therefore, the b…

medicine.medical_specialtyNifedipineNeuromuscular JunctionMollusk Venomschemistry.chemical_elementIn Vitro TechniquesCalciumN-type calcium channelMotor Endplatecomplex mixturesNeuromuscular junctionNifedipineomega-Conotoxin GVIAInternal medicinemedicineAnimalsL-type calcium channelVoltage-dependent calcium channelChemistryGeneral NeuroscienceCalcium channelRats Inbred StrainsCalcium Channel BlockersAcetylcholineElectric StimulationRatsReceptors AdrenergicPhrenic Nervemedicine.anatomical_structureEndocrinologyCalcium ChannelsAcetylcholinemedicine.drugNeuroscience Letters
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Effect of cocaine and related drugs on the uptake of noradrenaline by heart and spleen

1961

Noradrenaline uptake by heart and spleen after intravenous infusion of noradrenaline was measured in the pithed rat. Cocaine, given before the infusion, inhibited the noradrenaline uptake in relation (a) to the dose administered and (b) to the amount of noradrenaline infused. There was an association between increase in the pressor response to a test dose of noradrenaline and inhibition of the uptake by the heart. Drugs related chemically to cocaine, such as alpha-cocaine, amethocaine, and atropine, did not alter the noradrenaline uptake or potentiate the blood pressure response to noradrenaline. The noradrenaline uptake by the heart was unchanged after dibenamine, but blocked by the dichlo…

medicine.medical_specialtyNoradrenaline uptakeAdrenergic receptorAdrenergicSpleenPharmacologyNorepinephrineCocaineIsoprenalineInternal medicinemedicineAnimalsVasoconstrictor AgentsReceptorChemistryMyocardiumIsoproterenolHeartGeneral MedicineArticlesRatsReceptors AdrenergicAtropinemedicine.anatomical_structureEndocrinologyBlood pressureSpleenmedicine.drug
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Modulatory role of a constitutively active population of α1D-adrenoceptors in conductance arteries

2002

A constitutively active population of α1D-adrenoceptors in iliac and proximal, distal, and small mesenteric rat arteries was studied. The increase in resting tone (IRT) that evidences it was observed only in iliac and proximal mesenteric and was inhibited by prazosin (pIC50 = 9.57), 5-methylurapidil (pIC50 = 7.61), and BMY 7378 (pIC50 = 8.77). Chloroethylchlonidine (100 μmol/l) did not affect IRT, but when added before the other antagonists it blocked their effect. The potency shown by BMY 7378 confirms the α1D-subtype as responsible for IRT. BMY 7378 displayed greater inhibition of adrenergic responses in iliac (pIC50 = 7.57 ± 0.11) and proximal mesenteric arteries (pIC50 = 8.05 ± 0.2) th…

medicine.medical_specialtyPhysiologyPopulationConstitutively activeIliac ArteryClonidinePiperazinesContractilityNorepinephrineNorepinephrineReceptors Adrenergic alpha-1Physiology (medical)Internal medicinemedicineAnimalsRats WistareducationAdrenergic alpha-AntagonistsAortaeducation.field_of_studyDose-Response Relationship DrugChemistryConductanceArteriesPrazosinMesenteric ArteriesRatsmedicine.anatomical_structureEndocrinologyCirculatory systemCatecholamineCalciumFemaleVascular ResistanceCardiology and Cardiovascular MedicineAdrenergic alpha-AgonistsBlood vesselmedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Autonomic nervous control of the urinary bladder

2013

The autonomic nervous system plays an important role in the regulation of the urinary bladder function. Under physiological circumstances, noradrenaline, acting mainly on β(3) -adrenoceptors in the detrusor and on α(1) (A) -adrenoceptors in the bladder outflow tract, promotes urine storage, whereas neuronally released acetylcholine acting mainly on M(3) receptors promotes bladder emptying. Under pathophysiological conditions, however, this system may change in several ways. Firstly, there may be plasticity at the levels of innervation and receptor expression and function. Secondly, non-neuronal acetylcholine synthesis and release from the urothelium may occur during the storage phase, leadi…

medicine.medical_specialtyPhysiologyReceptor expressionUrinary Bladder030232 urology & nephrologyAdrenergicBiologyurologic and male genital diseasesAutonomic Nervous System03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptorReceptors Adrenergic betamedicineAnimalsHumansUrotheliumUrinary bladderNeuronal PlasticityUrinary Bladder DiseasesMuscarinic acetylcholine receptor M3Receptors Muscarinicfemale genital diseases and pregnancy complicationsAutonomic nervous systemmedicine.anatomical_structureEndocrinology030217 neurology & neurosurgeryAcetylcholinemedicine.drugActa Physiologica
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The metabolic syndrome in hypertension: European society of hypertension position statement.

2008

The metabolic syndrome considerably increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. Obesity and insulin resistance, beside a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with proinflammatory properties, have been implicated in the pathogenesis. The close relationships among the different components of the syndrome and their associated disturbances make it difficult to understand what the underlying causes and consequences are. At each of these …

medicine.medical_specialtyPhysiologySodium Chloride Symporter InhibitorsAdrenergic beta-AntagonistsPhysical exerciseAngiotensin-Converting Enzyme InhibitorsType 2 diabetesBioinformaticsInsulin resistanceWeight lossInternal medicineInternal MedicinemedicineHumansThiazideAntihypertensive AgentsMetabolic Syndromebusiness.industrymedicine.diseaseCalcium Channel BlockersObesityExercise TherapyEndocrinologyBlood pressureHypertensionmedicine.symptomMetabolic syndromeCardiology and Cardiovascular MedicinebusinessAngiotensin II Type 1 Receptor BlockersRisk Reduction Behaviormedicine.drugDiet TherapyJournal of hypertension
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Can you blame cold feet on Epac (and Rap1A)? Focus on “Cyclic AMP-Rap1A signaling activates RhoA to induce α2C-adrenoceptor translocation to the cell…

2012

Intracellular signaling by the second messenger cyclic AMP (cAMP) activates the Ras-related small GTPase Rap1 through the guanine exchange factor Epac. This activation leads to effector protein interactions, activation, and biological responses in the vasculature, including vasorelaxation. In vascular smooth muscle cells derived from human dermal arterioles (microVSM), Rap1 selectively regulates expression of G protein-coupled α2C-adrenoceptors (α2C-ARs) through JNK-c-jun nuclear signaling. The α2C-ARs are generally retained in the trans-Golgi compartment and mobilize to the cell surface and elicit vasoconstriction in response to cellular stress. The present study used human microVSM to exa…

medicine.medical_specialtyRHOAPhysiologyMyocytes Smooth MuscleCellChromosomal translocationSmooth muscleReceptors Adrenergic alpha-2Internal medicineCyclic AMPmedicineAnimalsHumansReceptorbiologyrap1 GTP-Binding ProteinsArticlesCell Biologyα2c adrenoceptorCell biologyProtein Transportmedicine.anatomical_structureEndocrinologybiology.proteinmedicine.symptomrhoA GTP-Binding ProteinVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Response to dopamine agonists of the rat isolated uterus.

1993

1. Quinpirole did not produce any effect in isolated uterus from oestrogenized rats even when it is contracted by KCl (37 mM). 2. Fenoldopam produced a relaxant effect on rat isolated uterus contracted by KCl which was not significantly modified by SCH 23390. 3. Reserpine decreased the effect of the lowest doses of fenoldopam. In reserpinized rats, propranolol (10(-9), 10(-8), 10(-7) M) antagonized the effect of the lowest doses of fenoldopam and neither SCH 23390, sulpiride nor ranitidine modified the effect of fenoldopam. 4. The results confirm our previous finding that DA1-receptors are not functional in our preparation. The effect of fenoldopam was partially due to a catecholamine-relea…

medicine.medical_specialtySerotoninQuinpiroleReserpineFenoldopamDopamine AgentsUterusPropranololPharmacologyFenoldopamIn Vitro TechniquesDopamine agonistchemistry.chemical_compoundUterine ContractionQuinpiroleCatecholaminesInternal medicineReceptors Adrenergic betamedicineAnimalsErgolinesRats WistarPharmacologySCH-23390ChemistryReserpineAcetylcholineRatsEndocrinologymedicine.anatomical_structureFemale2345-Tetrahydro-78-dihydroxy-1-phenyl-1H-3-benzazepineSulpiridemedicine.drugGeneral pharmacology
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D2-dopamine receptor blockade modulates temporal resolution in goldfish.

2002

A possible effect of dopamine on the temporal resolution of goldfish was investigated in a behavioral, two-alternative, forced-choice procedure. Flicker fusion frequency (FFF) was measured before and after bilateral intravitreal injections of D1- or D2-dopamine receptor (D1-/D2-R) antagonists, or after depletion of retinal dopamine by bilateral intravitreal injections of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA). Prior to drug injections, fish achieved FFFs of 33–39 Hz. A D1-R antagonist, SCH 23390, reduced FFF by about 12% (P > 0.1), whereas a D2 antagonist, sulpiride, reduced the relative FFF by 25% (P < 0.03). Depletion of retinal dopamine with 6-OHDA induced a gradual…

medicine.medical_specialtySerotoninTime FactorsTyrosine 3-MonooxygenasePhysiologyBiologyChoice BehaviorRetinaFlicker Fusionchemistry.chemical_compoundAdrenergic AgentsDopamineInternal medicineGoldfishmedicineNeurotoxinAnimalsOxidopamineSCH-23390Behavior AnimalAdaptation OcularReceptors Dopamine D2DopaminergicAntagonistRetinalBenzazepinesImmunohistochemistrySensory SystemsDopamine D2 Receptor AntagonistsEndocrinologychemistryDopamine receptorConditioning OperantDopamine AntagonistsSulpirideSulpiridemedicine.drugVisual neuroscience
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Safety and tolerability of β3-adrenoceptor agonists in the treatment of overactive bladder syndrome - insight from transcriptosome and experimental s…

2016

We have reviewed the safety and tolerability of β3-adrenoceptor agonists, specifically mirabegron and solabegron, a newly emerging drug class for the treatment of the overactive bladder syndrome. We discuss them mechanistically in the context of expression and other preclinical data.Based on a systematic PubMed search, incidence of overall adverse events, hypertension, dry mouth, and constipation are comparable between mirabegron or solabegron and placebo. Hypertension is the most frequently observed adverse event, but has a similar incidence with mirabegron and placebo. Nevertheless, severe uncontrolled hypertension has become a contraindication for use of mirabegron based on observation o…

medicine.medical_specialtySide effect030232 urology & nephrologyUrologyContext (language use)Adrenergic beta-3 Receptor AgonistsBenzoates03 medical and health sciences0302 clinical medicineSolabegronmedicineAnimalsHumansPharmacology (medical)Adverse effectAniline Compoundsbusiness.industryUrinary Bladder OveractiveGene Expression ProfilingBiphenyl CompoundsGeneral MedicineBiphenyl compoundThiazolesTolerability030220 oncology & carcinogenesisAnesthesiaReceptors Adrenergic beta-3AcetanilidesTolterodinebusinessMirabegronmedicine.drugExpert opinion on drug safety
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Pharmacotherapy of female urinary incontinence

2005

Urinary incontinence is a major clinical problem and a significant cause of disability and dependency in older adults. Overall, the prevalence of urinary incontinence approaches 55% among women aged over 55 years. The past few years have seen significant advances in the pharmacotherapy of overactive bladder and stress incontinence. The review examines the evidence regarding their benefits and side-effects.

medicine.medical_specialtyStress incontinencebusiness.industryHealth StatusUrinary Incontinence StressAnti-Infective Agents UrinaryUrologyObstetrics and GynecologyEstrogensUrinary incontinenceMuscarinic AntagonistsMiddle Agedmedicine.diseaseAdrenergic AgonistsCholinergic AntagonistsPharmacotherapyOveractive bladderInternal medicineQuality of LifeHumansWomen's HealthMedicineFemalemedicine.symptombusinessBritish Menopause Society Journal
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