Search results for " ADR"

showing 10 items of 285 documents

Hiperaldosteronismo primario por hiperplasia suprarrenal unilateral con resolución quirúrgica

2016

Unilateral adrenal hyperplasia is a rare cause of primary hyperaldosteronism (around a 3%) that has surgical treatment. A case of a patient with hypertension resistant to conventional therapy in treatment with 7 drugs who presented with primary hyperaldosteronism due to unilateral adrenal hyperplasia is presented. A left adrenalectomy was performed, and the patient had a good clinical response, with no need of any drug after 2 years of surgery. Unilateral adrenal hyperplasia is a different entity and it is not an asymmetric variant of the bilateral adrenal hyperplasia. In the study of patients with primary hyperaldosteronism and imaging tests with absence of adenoma is a diagnosis that must…

medicine.medical_specialtyMedical treatmentAdenomabusiness.industryLeft adrenalectomy030209 endocrinology & metabolism030204 cardiovascular system & hematologyHyperplasiamedicine.diseaseHyperaldosteronism03 medical and health sciences0302 clinical medicineInternal MedicineMedicineRadiologyCardiology and Cardiovascular MedicinebusinessSurgical treatmentHipertensión y Riesgo Vascular
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Cardiac biomarkers and arterial stiffening: data from the Gutenberg Health study

2013

medicine.medical_specialtyMyocardial ischemiabusiness.industryCardiac biomarkersmedicine.diseaseStiffeningMultiple Endocrine Neoplasia Type 2aInternal medicineArterial stiffnessCardiologyPhysical therapyMedicineMid regional pro adrenomedullinCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
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Beta-adrenoceptor stimulation enhances transmitter output from the rat phrenic nerve.

1988

Abstract 1. Neurally-evoked output of newly synthesized [3H]-acetylcholine from the rat phrenic nerve was measured in the absence of cholinesterase inhibitors. 2. Noradrenaline and isoprenaline enhanced neurally-evoked transmitter output markedly. Moreover, immediately after the application of noradrenaline the basal tritium efflux increased significantly. 3. Pretreatment with propranolol (0.1 mumol l-1) or atenolol (0.3 mumol l-1) completely prevented the stimulatory effect of noradrenaline and isoprenaline on evoked transmitter output. 4. The facilitatory effect of isoprenaline declined, when the exposure time was increased. This observation supports the assumption that beta-adrenoceptors…

medicine.medical_specialtyNeuromuscular transmissionMotor nerveStimulationIn Vitro Techniqueschemistry.chemical_compoundNorepinephrineInternal medicineIsoprenalineReceptors Adrenergic betamedicineAnimalsNeurotransmitterPhrenic nervePharmacologyNeurotransmitter Agentsbusiness.industryIsoproterenolRats Inbred StrainsAtenololPropranololRatsPhrenic NerveEndocrinologymedicine.anatomical_structurechemistryAtenololPeripheral nervous systembusinessmedicine.drugResearch Article
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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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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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Dual-release hydrocortisone improves hepatic steatosis in patients with secondary adrenal insufficiency: A real-life study

2019

Background:Conventional glucocorticoid treatment has a significant impact on liver in patients with adrenal insufficiency. Dual-release hydrocortisone (DR-HC) provides physiological cortisol exposure, leading to an improvement in anthropometric and metabolic parameters. We aimed to evaluate the effects of 12-month DR-HC treatment on the hepatic steatosis index (HSI), a validated surrogate index of hepatic steatosis, in patients with secondary adrenal insufficiency (SAI).Methods:A total of 45 patients with hypopituitarism, 22 with hypogonadism, hypothyroidism, ACTH, and GH deficiencies, and 23 with hypogonadism, hypothyroidism, and ACTH deficiency, on replacement therapy for all the pituitar…

medicine.medical_specialtySecondary adrenal insufficiencyEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismHypopituitarismHepatic steatosilcsh:Diseases of the endocrine glands. Clinical endocrinologyHypopituitarismSettore MED/13 - Endocrinologia03 medical and health sciences0302 clinical medicineInternal medicinemedicineAdrenal insufficiencyIn patientHydrocortisoneOriginal Researchlcsh:RC648-665business.industryhepatic steatosismedicine.diseaseInsulin sensitivityEndocrinology030220 oncology & carcinogenesisDual-release hydrocortisoneSteatosisLife studybusinessGlucocorticoidmedicine.drugSecondary adrenal insufficiency
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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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