Definitions
Wikipedia
Web
Articles
FAQWakefulness-Promoting Agents: A specific category of drugs that prevent sleepiness by specifically targeting sleep-mechanisms in the brain. They are used to treat DISORDERS OF EXCESSIVE SOMNOLENCE such as NARCOLEPSY. Note that this drug category does not include broadly-acting central nervous system stimulants such as AMPHETAMINES.Receptors, Adrenergic, alpha-2: A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.Interleukin 1 Receptor Antagonist Protein: A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.Neurokinin-1 Receptor Antagonists: Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.Purinergic P1 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Histamine H2 Antagonists: Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood.Serotonin 5-HT3 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT3 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT3 RECEPTOR AGONISTS.Piperidines: A family of hexahydropyridines.Excitatory Amino Acid Antagonists: Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.Dopamine Antagonists: Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.Serotonin 5-HT2 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT2 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT2 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more specific 5-HT2 receptor subtypes.Adenosine A2 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.Hormone Antagonists: Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.Adenosine A1 Receptor Antagonists: Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.Purinergic P2 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Narcotic Antagonists: Agents inhibiting the effect of narcotics on the central nervous system.Histamine H1 Antagonists: Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.Receptors, Endothelin: Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.Muscarinic Antagonists: Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.GABA-A Receptor Antagonists: Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.Adrenergic alpha-1 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.Serotonin Antagonists: Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or SEROTONIN RECEPTOR AGONISTS.GABA Antagonists: Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.Sialoglycoproteins: Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.Histamine Antagonists: Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.Receptors, Adrenergic, alpha: One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.Leukotriene Antagonists: A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.Receptor, Endothelin A: A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.Receptors, Serotonin: Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.Receptors, N-Methyl-D-Aspartate: A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.Serotonin 5-HT1 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT1 RECEPTORS, thereby blocking the actions of SEROTONIN 5-HT1 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more of the specific 5-HT1 receptor subtypes.Nicotinic Antagonists: Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.Dizocilpine Maleate: A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.Receptors, Interleukin-1: Cell surface receptors that are specific for INTERLEUKIN-1. Included under this heading are signaling receptors, non-signaling receptors and accessory proteins required for receptor signaling. Signaling from interleukin-1 receptors occurs via interaction with SIGNAL TRANSDUCING ADAPTOR PROTEINS such as MYELOID DIFFERENTIATION FACTOR 88.Adrenergic alpha-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.Adrenergic alpha-Antagonists: Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.Biphenyl CompoundsBenzazepines: Compounds with BENZENE fused to AZEPINES.TetrazolesRadioligand Assay: Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Xanthines: Purine bases found in body tissues and fluids and in some plants.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Serotonin Receptor Agonists: Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.Peptides, Cyclic: Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).Sulfonamides: A group of compounds that contain the structure SO2NH2.Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.Indoles: Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.Histamine H3 Antagonists: Drugs that selectively bind to but do not activate HISTAMINE H3 RECEPTORS. They have been used to correct SLEEP WAKE DISORDERS and MEMORY DISORDERS.Binding, Competitive: The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.Pyrazoles: Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.Hypoxia-Inducible Factor 1, alpha Subunit: Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.QuinoxalinesCells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Azepines: Seven membered heterocyclic rings containing a NITROGEN atom.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Endothelin-1: A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)GABA-B Receptor Antagonists: Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.alpha7 Nicotinic Acetylcholine Receptor: A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Receptors, Bradykinin: Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.Receptors, Neurokinin-1: A class of cell surface receptors for TACHYKININS with a preference for SUBSTANCE P. Neurokinin-1 (NK-1) receptors have been cloned and are members of the G protein coupled receptor superfamily. They are found on many cell types including central and peripheral neurons, smooth muscle cells, acinar cells, endothelial cells, fibroblasts, and immune cells.Adenosine A3 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.Receptor, Endothelin B: A subtype of endothelin receptor found predominantly in the KIDNEY. It may play a role in reducing systemic ENDOTHELIN levels.Purinergic P2X Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2X RECEPTORS. Included under this heading are antagonists for specific P2X receptor subtypes.PiperazinesBehavior, Animal: The observable response an animal makes to any situation.PyrrolidinesReceptors, Adrenergic, alpha-1: A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.Interleukin-1: A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.Receptors, Cholecystokinin: Cell surface proteins that bind cholecystokinin (CCK) with high affinity and trigger intracellular changes influencing the behavior of cells. Cholecystokinin receptors are activated by GASTRIN as well as by CCK-4; CCK-8; and CCK-33. Activation of these receptors evokes secretion of AMYLASE by pancreatic acinar cells, acid and PEPSIN by stomach mucosal cells, and contraction of the PYLORUS and GALLBLADDER. The role of the widespread CCK receptors in the central nervous system is not well understood.Devazepide: A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.Adrenergic Antagonists: Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.Receptors, Thromboxane: Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.Receptors, Vasopressin: Specific molecular sites or proteins on or in cells to which VASOPRESSINS bind or interact in order to modify the function of the cells. Two types of vasopressin receptor exist, the V1 receptor in the vascular smooth muscle and the V2 receptor in the kidneys. The V1 receptor can be subdivided into V1a and V1b (formerly V3) receptors.Ketanserin: A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.2-Amino-5-phosphonovalerate: The D-enantiomer is a potent and specific antagonist of NMDA glutamate receptors (RECEPTORS, N-METHYL-D-ASPARTATE). The L form is inactive at NMDA receptors but may affect the AP4 (2-amino-4-phosphonobutyrate; APB) excitatory amino acid receptors.Serotonin 5-HT4 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT4 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN RECEPTOR AGONISTS.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Receptor, Cannabinoid, CB1: A subclass of cannabinoid receptor found primarily on central and peripheral NEURONS where it may play a role modulating NEUROTRANSMITTER release.Benzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.Mice, Inbred C57BLReceptors, Dopamine D2: A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.Injections, Intraventricular: Injections into the cerebral ventricles.Adrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Famotidine: A competitive histamine H2-receptor antagonist. Its main pharmacodynamic effect is the inhibition of gastric secretion.Receptors, Neurokinin-2: A class of cell surface receptors for tachykinins that prefers neurokinin A; (NKA, substance K, neurokinin alpha, neuromedin L), neuropeptide K; (NPK); or neuropeptide gamma over other tachykinins. Neurokinin-2 (NK-2) receptors have been cloned and are similar to other G-protein coupled receptors.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Bradykinin: A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.Cannabinoid Receptor Antagonists: Compounds that inhibit or block the activity of CANNABINOID RECEPTORS.Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.QuinuclidinesBenzodiazepinonesHistamine: An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.Adrenergic beta-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.Bicuculline: An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.Receptors, Nicotinic: One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Interleukin-1alpha: An interleukin-1 subtype that occurs as a membrane-bound pro-protein form that is cleaved by proteases to form a secreted mature form. Unlike INTERLEUKIN-1BETA both membrane-bound and secreted forms of interleukin-1alpha are biologically active.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Receptors, Histamine H3: A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H3 receptors were first recognized as inhibitory autoreceptors on histamine-containing nerve terminals and have since been shown to regulate the release of several neurotransmitters in the central and peripheral nervous systems. (From Biochem Soc Trans 1992 Feb;20(1):122-5)Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.Receptors, Opioid: Cell membrane proteins that bind opioids and trigger intracellular changes which influence the behavior of cells. The endogenous ligands for opioid receptors in mammals include three families of peptides, the enkephalins, endorphins, and dynorphins. The receptor classes include mu, delta, and kappa receptors. Sigma receptors bind several psychoactive substances, including certain opioids, but their endogenous ligands are not known.
(1/356) alpha1-adrenergic receptor subtypes in human peripheral blood lymphocytes.
We investigated the expression of alpha1-adrenergic receptor subtypes in intact human peripheral blood lymphocytes using reverse transcription-polymerase chain reaction (RT-PCR) and radioligand binding assay techniques combined with antibodies against the three subtypes of alpha1-adrenergic receptors (alpha1A, alpha1B, and alpha1D). RT-PCR amplified in peripheral blood lymphocytes a 348-bp alpha1A-adrenergic receptor fragment, a 689-bp alpha1B-adrenergic receptor fragment, and a 540-bp alpha1D-adrenergic receptor fragment. Radioligand binding assay with [3H]prazosin as radioligand revealed a high-affinity binding with a dissociation constant value of 0. 65+/-0.05 nmol/L and a maximum density of binding sites of 175. 3+/-20.5 fmol/10(6) cells. The pharmacological profile of [3H]prazosin binding to human peripheral blood lymphocytes was consistent with the labeling of alpha1-adrenergic receptors. Antibodies against alpha1A-, alpha1B-, and alpha1D-receptor subtypes decreased [3H]prazosin binding to a different extent. This indicates that human peripheral blood lymphocytes express the three alpha1-adrenergic receptor subtypes. Of the three different alpha1-adrenergic receptor subtypes, the alpha1B is the most represented and the alpha1D, the least. Future studies should clarify the functional relevance of alpha1-adrenergic receptors expressed by peripheral blood lymphocytes. The identification of these sites may represent a step for evaluating whether they represent a marker of alpha1-adrenergic receptors in cardiovascular disorders or for assessing responses to drug treatment on these receptors. (+info)
(2/356) Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors.
In rat-1 fibroblasts stably expressing alpha1d-adrenoceptors BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil decreased basal [Ca2+]i. WB 4101 induced a very small effect on this parameter but when added before the other antagonists it blocked their effect. All these agents inhibited the action of norepinephrine. Phorbol myristate acetate also blocked the effect of norepinephrine and decreased basal [Ca2+]i. Staurosporine inhibited these effects of the phorbol ester. Our results suggest that: (1) alpha1d-adrenoceptors exhibit spontaneous ligand-independent activity, (2) BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil act as inverse agonists and (3) protein kinase C activation blocks spontaneous and agonist-stimulated alpha1d-adrenoceptor activity. (+info)
(3/356) Characterization of alpha1-adrenoceptor subtypes mediating vasoconstriction in human umbilical vein.
1. The present study attempted to characterize pharmacologically the subtypes of alpha-adrenoceptors mediating contractions in human umbilical vein (HUV). 2. HUV rings were mounted in isolated organ baths and cumulative concentration-response curves were constructed for the alpha-adrenoceptor agonists phenylephrine and adrenaline. Adrenaline was more potent than phenylephrine (pD2=7.29 and 6.04 respectively). 3. Isoproterenol exhibited no agonism on KCl pre-contracted HUV rings. Propranolol (1 microM) and rauwolscine (0.1 microM) did not affect the concentration-response curves to adrenaline. These results demonstrate the lack of involvement of functional beta-or alpha2-adrenoceptors in adrenaline-induced vasoconstriction. 4. The non subtype selective alpha1-adrenoceptor antagonist prazosin was evaluated on phenylephrine and adrenaline concentration-response curves. The effects of the competitive alpha1A and alpha1D-adrenoceptor antagonists, 5-methyl urapidil and BMY 7378 and the irreversible alpha1B selective compound chloroethylclonidine (CEC) were also evaluated on adrenaline concentration-response curves. 5. The potencies of prazosin against responses mediated by adrenaline (pA2= 10.87) and phenylephrine (pA2= 10.70) indicate the involvement of prazosin-sensitive functional alpha1-adrenoceptor subtype in vasoconstriction of the HUV. 6. The potencies of 5-methyl urapidil (pA2 = 6.70) and BMY 7378 (pA2= 7.34) were not consistent with the activation of an alpha1A- or alpha1D-adrenoceptor population. 7. Exposure to a relatively low CEC concentration (3 microM) abolished the maximum response to adrenaline suggesting that this response was mediated by an alpha1B-adrenoceptor subtype. 8. We conclude that HUV express a prazosin-sensitive functional alpha1-adrenoceptor resembling the alpha1B-subtype according with the low pA2 values for both 5-methyl urapidil and BMY 7378 and the high sensitivity to CEC. (+info)
(4/356) Comparison of relaxation responses of cavernous and trigonal smooth muscles from rabbits by alpha1-adrenoceptor antagonists; prazosin, terazosin, doxazosin, and tamsulosin.
Alpha1a-adrenergic receptor (AR) primarily mediates the contraction of the prostatic and cavernous smooth muscles. Among clinically available alpha1-AR antagonists for the medical management of benign prostatic hyperplasia (BPH), tamsulosin has a modest selectivity for alpha1A- and alpha1D- over alpha1B-ARs. To compare the effects of various alpha1-AR antagonists on relaxation responses of cavernous and trigonal smooth muscles, isometric tension studies with relatively selective (tamsulosin) and non-selective (prazosin, doxazosin, and terazosin) alpha1A-AR antagonists, were conducted in the cavernous and trigonal muscle strips of rabbits (n=10 each). Tamsulosin had the strongest inhibitory effect on contraction of trigonal smooth muscle among the various alpha1-AR antagonists, and the inhibitory activities of prazosin, doxazosin, and terazosin were not statistically different. All alpha1-AR antagonists caused concentration-dependent relaxation of the cavernous muscle strips. Tamsulosin was shown to have greater potency than prazosin (more than 100-fold), doxazosin (more than 1000-fold), and terazosin (more than 1000-fold), in relaxation of cavernous smooth muscle. In conclusion, tamsulosin might be the most effective drug among the four commonly used alpha1-AR antagonists for the medical management of BPH. Tamsulosin might be a potential substitute for phentolamine in combination with vasoactive agents as an intracavernous injection therapy for patients with erectile dysfunction. (+info)
(5/356) Canine external carotid vasoconstriction to methysergide, ergotamine and dihydroergotamine: role of 5-HT1B/1D receptors and alpha2-adrenoceptors.
The antimigraine drugs methysergide, ergotamine and dihydroergotamine (DHE) produce selective vasoconstriction in the external carotid bed of vagosympathectomized dogs anaesthetized with pentobarbital and artificially respired, but the receptors involved have not yet been completely characterized. Since the above drugs display affinity for several binding sites, including alpha-adrenoceptors and several 5-HT1 and 5-HT2 receptor subtypes, this study has analysed the mechanisms involved in the above responses. Intracarotid (i.c.) infusions during 1 min of methysergide (31-310 microg min(-1)), ergotamine (0.56-5.6 microg min(-1)) or DHE (5.6-31 microg min(-1)) dose-dependently reduced external carotid blood flow (ECBF) by up to 46+/-4, 37+/-4 and 49+/-5%, respectively. Blood pressure and heart rate remained unchanged. The reductions in ECBF by methysergide were abolished and even reversed to increases in animals pre-treated with GR127935 (10 microg kg(-1), i.v.). The reductions in ECBF by ergotamine and DHE remained unchanged in animals pre-treated (i.v.) with prazosin (300 microg kg(-1)), but were partly antagonized in animals pre-treated with either GR127935 (10 or 30 microg kg(-1)) or yohimbine (1000 microg kg(-1)). Pre-treatment with a combination of GR127935 (30 microg kg(-1)) and yohimbine (1000 microg kg(-1)) abolished the responses to both ergotamine and DHE. The above doses of antagonists were shown to produce selective antagonism at their respective receptors. These results suggest that the external carotid vasoconstrictor responses to methysergide primarily involve 5-HT1B/1D receptors, whereas those to ergotamine and DHE are mediated by 5-HT1B/1D receptors as well as alpha2-adrenoceptors. (+info)
(6/356) alpha1-adrenergic receptor activation of c-fos expression in transfected rat-1 fibroblasts: role of Ca2+.
alpha1-Adrenergic receptors mediate mitogenic responses and increase intracellular free Ca2+ ([Ca2+]i) in vascular smooth muscle cells. Induction of c-fos is a critical early event in cell growth; expression of this gene is regulated by a number of signaling pathways including Ca2+. We wondered whether Ca2+ signaling plays a critical role in the induction of c-fos gene by alpha1-adrenergic receptors. Using stably transfected rat-1 fibroblasts, we confirmed that PE induced c-fos mRNA expression in a time- and dose-dependent manner, and also increased [Ca2+]i (measured with Fura-2 AM). These responses were blocked by the alpha1-adrenergic receptor antagonist doxazosin. Both intracellular Ca2+ chelation (using BAPTA/AM) and extracellular Ca2+ depletion (using EGTA) significantly inhibited PE-induced c-fos expression by alpha1A and alpha1B receptors. Brief (1-min) stimulation of alpha1A and alpha1B receptors with PE did not maximally induce c-fos expression, suggesting that a sustained increase in [Ca2+]i due to Ca2+ influx is required. The calmodulin (CaM) antagonists, R24571, W7, and trifluoperazine, but not the CaM-dependent protein kinases inhibitor KN-62, significantly inhibited c-fos induction by alpha1A and alpha1B receptors. Neither inhibition of protein kinase C nor inhibition of adenylyl cyclase modified c-fos induction by PE. These results suggest that alpha1-adrenergic receptor-induced c-fos expression in rat-1 cells is dependent on a Ca2+/CaM-associated pathway. (+info)
(7/356) In vivo measurement by [3H]Tamsulosin of alpha1 adrenoceptors in rat tissues in relation to the pharmacokinetics.
The present study was undertaken to simultaneously measure alpha1 adrenoceptors in rat tissues by [3H]tamsulosin in vivo. In vivo specific [3H]tamsulosin binding was observed in the prostate, vas deferens, aorta, submaxillary gland, spleen, heart, lung, and kidney after i.v. injection of the ligand but not in the cerebral cortex and liver. Specific [3H]tamsulosin binding in the kidney, lung, heart, and spleen was greatest at 3 min after i.v. injection and declined rapidly with the disappearance of [3H]tamsulosin from the plasma. On the other hand, [3H]tamsulosin binding in the prostate and aorta peaked at 10 to 60 min after i.v. injection, and a considerable level of specific binding in both tissues persisted up to 240 min. The most sustained binding of [3H]tamsulosin occurred in the submaxillary gland. In vivo specific [3H]tamsulosin binding in rat tissues was effectively inhibited by the coinjection of low doses of unlabeled tamsulosin, prazosin, and terazosin with the radioligand but not by relatively high doses of yohimbine and propranolol. Based on estimated ID50 values, in vivo inhibitory effect of tamsulosin compared with prazosin was 5 to 14 times greater in rat tissues except the spleen, which showed 1.6 times less potent than prazosin. From ratios of ID50 (spleen) to ID50 (submaxillary gland) or ID50 (prostate), tamsulosin was 9 and 19 times, respectively, greater than prazosin in selectivity of alpha1 adrenoceptors in the submaxillary gland and prostate versus the spleen, respectively, suggesting that tamsulosin binds to alpha1A subtype with higher affinity than alpha1B subtype in vivo. The present study suggests that [3H]tamsulosin is a useful radioligand for in vivo measurement of alpha1 adrenoceptors in rat tissues. (+info)
(8/356) Naftopidil, a novel alpha1-adrenoceptor antagonist, displays selective inhibition of canine prostatic pressure and high affinity binding to cloned human alpha1-adrenoceptors.
The pharmacological profiles of the alpha1-adrenoceptor antagonists naftopidil, tamsulosin and prazosin were studied in an anesthetized dog model that allowed the simultaneous assessment of their antagonist potency against phenylephrine-mediated increases in prostatic pressure and mean blood pressure. The intravenous administration of each of these compounds dose-dependently inhibited phenylephrine-induced increases in prostatic pressure and mean blood pressure. To further assess the ability of the three compounds to inhibit phenylephrine-induced responses, the doses required to produce a 50% inhibition of the phenylephrine-induced increases in prostatic and mean blood pressure and the selectivity index obtained from the ratio of those two doses were determined for each test compound. Forty minutes after the intravenous administration of naftopidil, the selectivity index was 3.76, and those of tamsulosin and prazosin were 1.23 and 0.61, respectively. These findings demonstrated that naftopidil selectively inhibited the phenylephrine-induced increase in prostatic pressure compared with mean blood pressure in the anesthetized dog model. The selectivity of naftopidil for prostatic pressure was the most potent among the test compounds. In addition, using cloned human alpha1-adrenoceptor subtypes, naftopidil was selective for the alpha1d-adrenoceptor with approximately 3- and 17-fold higher affinity than for the alpha1a- and alpha1b-adrenoceptor subtypes, respectively. The selectivity of naftopidil for prostatic pressure may be attributable to its high binding affinity for alpha1a- and alpha1d-adrenoceptor subtypes. (+info)
We investigated the expression of alpha1-adrenergic receptor subtypes in intact human peripheral blood lymphocytes using reverse transcription-polymerase chain reaction (RT-PCR) and radioligand binding assay techniques combined with antibodies against the three subtypes of alpha1-adrenergic receptors (alpha1A, alpha1B, and alpha1D). RT-PCR amplified in peripheral blood lymphocytes a 348-bp alpha1A-adrenergic receptor fragment, a 689-bp alpha1B-adrenergic receptor fragment, and a 540-bp alpha1D-adrenergic receptor fragment. Radioligand binding assay with [3H]prazosin as radioligand revealed a high-affinity binding with a dissociation constant value of 0. 65+/-0.05 nmol/L and a maximum density of binding sites of 175. 3+/-20.5 fmol/10(6) cells. The pharmacological profile of [3H]prazosin binding to human peripheral blood lymphocytes was consistent with the labeling of alpha1-adrenergic receptors. Antibodies against alpha1A-, alpha1B-, and alpha1D-receptor subtypes decreased [3H]prazosin binding to a different extent. This indicates that human peripheral blood lymphocytes express the three alpha1-adrenergic receptor subtypes. Of the three different alpha1-adrenergic receptor subtypes, the alpha1B is the most represented and the alpha1D, the least. Future studies should clarify the functional relevance of alpha1-adrenergic receptors expressed by peripheral blood lymphocytes. The identification of these sites may represent a step for evaluating whether they represent a marker of alpha1-adrenergic receptors in cardiovascular disorders or for assessing responses to drug treatment on these receptors. (+info)
(2/356) Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors.
In rat-1 fibroblasts stably expressing alpha1d-adrenoceptors BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil decreased basal [Ca2+]i. WB 4101 induced a very small effect on this parameter but when added before the other antagonists it blocked their effect. All these agents inhibited the action of norepinephrine. Phorbol myristate acetate also blocked the effect of norepinephrine and decreased basal [Ca2+]i. Staurosporine inhibited these effects of the phorbol ester. Our results suggest that: (1) alpha1d-adrenoceptors exhibit spontaneous ligand-independent activity, (2) BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil act as inverse agonists and (3) protein kinase C activation blocks spontaneous and agonist-stimulated alpha1d-adrenoceptor activity. (+info)
(3/356) Characterization of alpha1-adrenoceptor subtypes mediating vasoconstriction in human umbilical vein.
1. The present study attempted to characterize pharmacologically the subtypes of alpha-adrenoceptors mediating contractions in human umbilical vein (HUV). 2. HUV rings were mounted in isolated organ baths and cumulative concentration-response curves were constructed for the alpha-adrenoceptor agonists phenylephrine and adrenaline. Adrenaline was more potent than phenylephrine (pD2=7.29 and 6.04 respectively). 3. Isoproterenol exhibited no agonism on KCl pre-contracted HUV rings. Propranolol (1 microM) and rauwolscine (0.1 microM) did not affect the concentration-response curves to adrenaline. These results demonstrate the lack of involvement of functional beta-or alpha2-adrenoceptors in adrenaline-induced vasoconstriction. 4. The non subtype selective alpha1-adrenoceptor antagonist prazosin was evaluated on phenylephrine and adrenaline concentration-response curves. The effects of the competitive alpha1A and alpha1D-adrenoceptor antagonists, 5-methyl urapidil and BMY 7378 and the irreversible alpha1B selective compound chloroethylclonidine (CEC) were also evaluated on adrenaline concentration-response curves. 5. The potencies of prazosin against responses mediated by adrenaline (pA2= 10.87) and phenylephrine (pA2= 10.70) indicate the involvement of prazosin-sensitive functional alpha1-adrenoceptor subtype in vasoconstriction of the HUV. 6. The potencies of 5-methyl urapidil (pA2 = 6.70) and BMY 7378 (pA2= 7.34) were not consistent with the activation of an alpha1A- or alpha1D-adrenoceptor population. 7. Exposure to a relatively low CEC concentration (3 microM) abolished the maximum response to adrenaline suggesting that this response was mediated by an alpha1B-adrenoceptor subtype. 8. We conclude that HUV express a prazosin-sensitive functional alpha1-adrenoceptor resembling the alpha1B-subtype according with the low pA2 values for both 5-methyl urapidil and BMY 7378 and the high sensitivity to CEC. (+info)
(4/356) Comparison of relaxation responses of cavernous and trigonal smooth muscles from rabbits by alpha1-adrenoceptor antagonists; prazosin, terazosin, doxazosin, and tamsulosin.
Alpha1a-adrenergic receptor (AR) primarily mediates the contraction of the prostatic and cavernous smooth muscles. Among clinically available alpha1-AR antagonists for the medical management of benign prostatic hyperplasia (BPH), tamsulosin has a modest selectivity for alpha1A- and alpha1D- over alpha1B-ARs. To compare the effects of various alpha1-AR antagonists on relaxation responses of cavernous and trigonal smooth muscles, isometric tension studies with relatively selective (tamsulosin) and non-selective (prazosin, doxazosin, and terazosin) alpha1A-AR antagonists, were conducted in the cavernous and trigonal muscle strips of rabbits (n=10 each). Tamsulosin had the strongest inhibitory effect on contraction of trigonal smooth muscle among the various alpha1-AR antagonists, and the inhibitory activities of prazosin, doxazosin, and terazosin were not statistically different. All alpha1-AR antagonists caused concentration-dependent relaxation of the cavernous muscle strips. Tamsulosin was shown to have greater potency than prazosin (more than 100-fold), doxazosin (more than 1000-fold), and terazosin (more than 1000-fold), in relaxation of cavernous smooth muscle. In conclusion, tamsulosin might be the most effective drug among the four commonly used alpha1-AR antagonists for the medical management of BPH. Tamsulosin might be a potential substitute for phentolamine in combination with vasoactive agents as an intracavernous injection therapy for patients with erectile dysfunction. (+info)
(5/356) Canine external carotid vasoconstriction to methysergide, ergotamine and dihydroergotamine: role of 5-HT1B/1D receptors and alpha2-adrenoceptors.
The antimigraine drugs methysergide, ergotamine and dihydroergotamine (DHE) produce selective vasoconstriction in the external carotid bed of vagosympathectomized dogs anaesthetized with pentobarbital and artificially respired, but the receptors involved have not yet been completely characterized. Since the above drugs display affinity for several binding sites, including alpha-adrenoceptors and several 5-HT1 and 5-HT2 receptor subtypes, this study has analysed the mechanisms involved in the above responses. Intracarotid (i.c.) infusions during 1 min of methysergide (31-310 microg min(-1)), ergotamine (0.56-5.6 microg min(-1)) or DHE (5.6-31 microg min(-1)) dose-dependently reduced external carotid blood flow (ECBF) by up to 46+/-4, 37+/-4 and 49+/-5%, respectively. Blood pressure and heart rate remained unchanged. The reductions in ECBF by methysergide were abolished and even reversed to increases in animals pre-treated with GR127935 (10 microg kg(-1), i.v.). The reductions in ECBF by ergotamine and DHE remained unchanged in animals pre-treated (i.v.) with prazosin (300 microg kg(-1)), but were partly antagonized in animals pre-treated with either GR127935 (10 or 30 microg kg(-1)) or yohimbine (1000 microg kg(-1)). Pre-treatment with a combination of GR127935 (30 microg kg(-1)) and yohimbine (1000 microg kg(-1)) abolished the responses to both ergotamine and DHE. The above doses of antagonists were shown to produce selective antagonism at their respective receptors. These results suggest that the external carotid vasoconstrictor responses to methysergide primarily involve 5-HT1B/1D receptors, whereas those to ergotamine and DHE are mediated by 5-HT1B/1D receptors as well as alpha2-adrenoceptors. (+info)
(6/356) alpha1-adrenergic receptor activation of c-fos expression in transfected rat-1 fibroblasts: role of Ca2+.
alpha1-Adrenergic receptors mediate mitogenic responses and increase intracellular free Ca2+ ([Ca2+]i) in vascular smooth muscle cells. Induction of c-fos is a critical early event in cell growth; expression of this gene is regulated by a number of signaling pathways including Ca2+. We wondered whether Ca2+ signaling plays a critical role in the induction of c-fos gene by alpha1-adrenergic receptors. Using stably transfected rat-1 fibroblasts, we confirmed that PE induced c-fos mRNA expression in a time- and dose-dependent manner, and also increased [Ca2+]i (measured with Fura-2 AM). These responses were blocked by the alpha1-adrenergic receptor antagonist doxazosin. Both intracellular Ca2+ chelation (using BAPTA/AM) and extracellular Ca2+ depletion (using EGTA) significantly inhibited PE-induced c-fos expression by alpha1A and alpha1B receptors. Brief (1-min) stimulation of alpha1A and alpha1B receptors with PE did not maximally induce c-fos expression, suggesting that a sustained increase in [Ca2+]i due to Ca2+ influx is required. The calmodulin (CaM) antagonists, R24571, W7, and trifluoperazine, but not the CaM-dependent protein kinases inhibitor KN-62, significantly inhibited c-fos induction by alpha1A and alpha1B receptors. Neither inhibition of protein kinase C nor inhibition of adenylyl cyclase modified c-fos induction by PE. These results suggest that alpha1-adrenergic receptor-induced c-fos expression in rat-1 cells is dependent on a Ca2+/CaM-associated pathway. (+info)
(7/356) In vivo measurement by [3H]Tamsulosin of alpha1 adrenoceptors in rat tissues in relation to the pharmacokinetics.
The present study was undertaken to simultaneously measure alpha1 adrenoceptors in rat tissues by [3H]tamsulosin in vivo. In vivo specific [3H]tamsulosin binding was observed in the prostate, vas deferens, aorta, submaxillary gland, spleen, heart, lung, and kidney after i.v. injection of the ligand but not in the cerebral cortex and liver. Specific [3H]tamsulosin binding in the kidney, lung, heart, and spleen was greatest at 3 min after i.v. injection and declined rapidly with the disappearance of [3H]tamsulosin from the plasma. On the other hand, [3H]tamsulosin binding in the prostate and aorta peaked at 10 to 60 min after i.v. injection, and a considerable level of specific binding in both tissues persisted up to 240 min. The most sustained binding of [3H]tamsulosin occurred in the submaxillary gland. In vivo specific [3H]tamsulosin binding in rat tissues was effectively inhibited by the coinjection of low doses of unlabeled tamsulosin, prazosin, and terazosin with the radioligand but not by relatively high doses of yohimbine and propranolol. Based on estimated ID50 values, in vivo inhibitory effect of tamsulosin compared with prazosin was 5 to 14 times greater in rat tissues except the spleen, which showed 1.6 times less potent than prazosin. From ratios of ID50 (spleen) to ID50 (submaxillary gland) or ID50 (prostate), tamsulosin was 9 and 19 times, respectively, greater than prazosin in selectivity of alpha1 adrenoceptors in the submaxillary gland and prostate versus the spleen, respectively, suggesting that tamsulosin binds to alpha1A subtype with higher affinity than alpha1B subtype in vivo. The present study suggests that [3H]tamsulosin is a useful radioligand for in vivo measurement of alpha1 adrenoceptors in rat tissues. (+info)
(8/356) Naftopidil, a novel alpha1-adrenoceptor antagonist, displays selective inhibition of canine prostatic pressure and high affinity binding to cloned human alpha1-adrenoceptors.
The pharmacological profiles of the alpha1-adrenoceptor antagonists naftopidil, tamsulosin and prazosin were studied in an anesthetized dog model that allowed the simultaneous assessment of their antagonist potency against phenylephrine-mediated increases in prostatic pressure and mean blood pressure. The intravenous administration of each of these compounds dose-dependently inhibited phenylephrine-induced increases in prostatic pressure and mean blood pressure. To further assess the ability of the three compounds to inhibit phenylephrine-induced responses, the doses required to produce a 50% inhibition of the phenylephrine-induced increases in prostatic and mean blood pressure and the selectivity index obtained from the ratio of those two doses were determined for each test compound. Forty minutes after the intravenous administration of naftopidil, the selectivity index was 3.76, and those of tamsulosin and prazosin were 1.23 and 0.61, respectively. These findings demonstrated that naftopidil selectively inhibited the phenylephrine-induced increase in prostatic pressure compared with mean blood pressure in the anesthetized dog model. The selectivity of naftopidil for prostatic pressure was the most potent among the test compounds. In addition, using cloned human alpha1-adrenoceptor subtypes, naftopidil was selective for the alpha1d-adrenoceptor with approximately 3- and 17-fold higher affinity than for the alpha1a- and alpha1b-adrenoceptor subtypes, respectively. The selectivity of naftopidil for prostatic pressure may be attributable to its high binding affinity for alpha1a- and alpha1d-adrenoceptor subtypes. (+info)
Bunazosin
Systemic Alpha-1 adrenergic receptor antagonists have been implicated in Intraoperative Floppy Iris Syndrome (IFIS). Bunazosin ... Bunazosin (INN) is an alpha 1 antagonist. Bunazosin was initially developed to treat benign prostatic hyperplasia (BPH). It has ...
Alpha-1 blocker
Silodosin shows high affinity and selectivity for alpha-1a adrenergic receptors found in the prostate which ensures that it ... Taylor, Fletcher; Raskind, Murray A. (February 2002). "The alpha1-adrenergic antagonist prazosin improves sleep and nightmares ... DrugDigest - Alpha blockers RxList.com - Tamsulosin alpha-Adrenergic Blockers at the US National Library of Medicine Medical ... Silodosin is the most selective for alpha-1a receptors. The affinity and selectivity for alpha-1 receptors seems to be ...
L-765,314
... a potent and selective alpha1b adrenergic receptor antagonist ". Journal of Medicinal Chemistry. 41 (8): 1205-8. doi:10.1021/ ... L-765,314 is a drug which acts as a potent and selective antagonist for the Alpha-1 adrenergic receptor subtype α1B. It has ... Yang XP, Chiba S (August 2002). "Effects of L-765,314, a selective and potent alpha 1B-adrenoceptor antagonist, on periarterial ... Hillman KL, Doze VA, Porter JE (June 2007). "Alpha1A-adrenergic receptors are functionally expressed by a subpopulation of ...
Tetrahydropalmatine
Additionally, l-THP displays significant binding to 5-HT1A and alpha-2 adrenergic receptors. In the case of 5-HT1A receptors, l ... at which it functions as an antagonist, and GABA-A receptors, through positive allosteric modulation. ... alpha adrenergic and serotonin receptors. The Ki values for l-THP at D1 and D2 dopamine receptors are approximately 124 nM (D1 ... Along with dopamine receptors, l-THP has been reported to interact with a number of other receptor types, including alpha-1 ...
2C-H
It features competitive antagonist activity at 5-HT serotonin receptor in Sprague-Dawley rat stomachs. It exhibits binding ... It was found to be an active Alpha-1 adrenergic receptor agonist in rabbit ear arteries. It has binding affinity towards 5-HT2C ... It exhibits agonist activity at human trace amine associated receptor 1 expressed in RD-HGA16 CHO-K1 cells coexpressed with ... affinity against rat 5-hydroxytryptamine 2C receptors using [3H]mesulergine as a radioligand. As of October 31, 2016; 2C-H is a ...
Alpha-1D adrenergic receptor
Antagonists A-315456 BMY 7378 (also α2C antagonist) Adrenergic receptor GRCh38: Ensembl release 89: ENSG00000171873 - Ensembl, ... This gene encodes alpha-1D-adrenergic receptor. Similar to alpha-1B-adrenergic receptor gene, this gene comprises 2 exons and a ... 1994). "Cloning, expression and characterization of human alpha adrenergic receptors alpha 1a, alpha 1b and alpha 1c". Biochem ... The alpha-1D adrenergic receptor (α1D adrenoreceptor), also known as ADRA1D, is an alpha-1 adrenergic receptor, and also ...
Adrenergic antagonist
This drug is a non-selective α-adrenergic antagonist, which means it binds to both alpha receptors. There are few if any ... An adrenergic antagonist is a drug that inhibits the function of adrenergic receptors. There are five adrenergic receptors, ... Adrenergic competitive antagonists are shorter lasting than the other two types of antagonists. While the antagonists for alpha ... There are few non-cardiovascular uses for adrenergic antagonists. Alpha-adrenergic antagonists are also used for treatment of ...
Alpha-1 adrenergic receptor
... relationships between alpha-adrenergic activity and binding affinity of alpha-adrenoceptor agonists and antagonists". Journal ... Note that only active muscle α1-adrenergic receptors will be blocked. Resting muscle will not have its α1-adrenergic receptors ... In contrast to α2-adrenergic receptors, α1-adrenergic-receptors in the arterial vasculature of skeletal muscle are more ... The α1-adrenergic receptor has several general functions in common with the α2-adrenergic receptor, but also has specific ...
Post-traumatic amnesia
Administering a norepinephrine receptor agonist (a substance that initiates a cell response when it binds with a receptor) to ... Noradrenergic antagonists were not prescribed for the purposes of slowing the recovery of memory. Rather, these findings are ... The alpha-1 adrenergic receptor is specifically implicated. Although it has not yet been thoroughly investigated, there is ... Conversely, the administration of norpinephrine antagonists slowed recovery, and could lead to the reinstatement of deficits ...
Alpha-2C adrenergic receptor
Cleary L, Murad K, Bexis S, Docherty JR (2005). "The alpha (1D)-adrenoceptor antagonist BMY 7378 is also an alpha (2C)- ... The alpha-2C adrenergic receptor (α2C adrenoceptor), also known as ADRA2C, is an alpha-2 adrenergic receptor, and also denotes ... "Human alpha 2-adrenergic receptor subtype distribution: widespread and subtype-selective expression of alpha 2C10, alpha 2C4, ... Alpha-2-adrenergic receptors include 3 highly homologous subtypes: alpha2A, alpha2B, and alpha2C. These receptors have a ...
Alpha-1B adrenergic receptor
Antagonists L-765,314 Risperidone Alpha-1B adrenergic receptor has been shown to interact with AP2M1. A role in regulation of ... 1994). "Cloning, expression and characterization of human alpha adrenergic receptors alpha 1a, alpha 1b and alpha 1c". Biochem ... The alpha-1B adrenergic receptor (α1B adrenoreceptor), also known as ADRA1B, is an alpha-1 adrenergic receptor, and also ... 2003). "The adaptor complex 2 directly interacts with the alpha 1b-adrenergic receptor and plays a role in receptor endocytosis ...
Alpha blocker
However, the most common type of alpha blocker is usually an α1 blocker. Non-selective α-adrenergic receptor antagonists ... are a class of pharmacological agents that act as antagonists on α-adrenergic receptors (α-adrenoceptors). Historically, alpha- ... "Alpha-Adrenoceptor Antagonists (Alpha-Blockers)" (PDF). British Hypertension Society. "CV Pharmacology , Alpha-Adrenoceptor ... and alpha 2-adrenergic receptors". The FASEB Journal. 6: 832-839. McKeage, Kate; Plosker, Greg L. (2002-03-01). "Alfuzosin". ...
Alpha-2A adrenergic receptor
... seventh hydrophobic domain of the alpha 2 adrenergic receptor increases its affinity for a family of beta receptor antagonists ... The alpha-2A adrenergic receptor (α2A adrenoceptor), also known as ADRA2A, is an α2 adrenergic receptor, and also denotes the ... the sites for beta-adrenergic receptor kinase-mediated phosphorylation and desensitization of the alpha 2A-adrenergic receptor ... ADRA2A adrenergic, alpha-2A-, receptor". "α2A-adrenoceptor". IUPHAR Database of Receptors and Ion Channels. International Union ...
Beta-2 adrenergic receptor
... denotes selective antagonist to the receptor. Beta-2 adrenergic receptor has been shown to interact with: AKAP12, OPRD1, Grb2, ... Other adrenergic receptors Alpha-1 adrenergic receptor Alpha-2 adrenergic receptor Beta-1 adrenergic receptor Beta-3 adrenergic ... The beta-2 adrenergic receptor (β2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor ... "Insulin stimulates sequestration of beta-adrenergic receptors and enhanced association of beta-adrenergic receptors with Grb2 ...
Beta-3 adrenergic receptor
... has been shown to interact with Src. Other adrenergic receptors Alpha-1 adrenergic receptor Alpha-2 ... Nisoli E, Tonello C, Landi M, Carruba MO (1996). "Functional studies of the first selective β3-adrenergic receptor antagonist ... The beta-3 adrenergic receptor (β3 adrenoreceptor), also known as ADRB3, is a beta-adrenergic receptor, and also denotes the ... adrenergic receptor antagonists". The Journal of Pharmacology and Experimental Therapeutics. 290 (2): 649-55. PMID 10411574. ...
Adrenergic receptor
ISBN 0-443-06911-5. Alpha receptors illustrated The Adrenergic Receptors "Adrenoceptors". IUPHAR Database of Receptors and Ion ... "Functional studies of the first selective beta 3-adrenergic receptor antagonist SR 59230A in rat brown adipocytes". Molecular ... Beta adrenergic receptor kinase Beta adrenergic receptor kinase-2 Cannon WB, Rosenbluth A (31 May 1933). "Studies On Conditions ... Basic Neurochemistry: α- and β-Adrenergic Receptors Brief overview of functions of the β3 receptor Theory of receptor ...
WB-4101
... is a compound which acts as an antagonist at the α1B-adrenergic receptor. It was one of the first selective antagonists ... Search for selective antagonists at alpha 1-adrenoreceptors: neutral or negative antagonism? Farmaco. 1998 Apr;53(4):278-86. ... developed for this receptor and was invented in 1969, but is still commonly used in research into adrenergic receptors, ... 1969 Mar;12(2):326-9. PMID 5791620 Morrow AL, Creese I. Characterization of alpha 1-adrenergic receptor subtypes in rat brain: ...
Vascular smooth muscle
See also receptor antagonist) α 2 {\displaystyle \alpha _{2}} receptors. Agonists of α 2 {\displaystyle \alpha _{2}} receptors ... The main endogenous agonist of these cell receptors is norepinephrine (NE). The adrenergic receptors exert opposite physiologic ... alpha _{2}} receptors in the vascular smooth muscle cells). Usage of β 2 {\displaystyle \beta _{2}} receptor agonists as ... However, in clinical practice drugs applied intravenously that are agonists of α 2 {\displaystyle \alpha _{2}} receptors ( ...
Bronchospasm
... all of which act as receptor antagonists of muscarinic acetylcholine receptors) are effective for treating asthma and COPD- ... Beta2-adrenergic agonists are recommended for bronchospasm. Short acting (SABA) Terbutaline Salbutamol Levosalbutamol Long ... Both of these medications activate alpha-1 adrenergic receptors that result in smooth muscle constriction. Non-selective beta ... Beta blockers bind into the β2 receptors and block the action of epinephrine and norepinephrine from binding to its receptors, ...
Monatepil
... is a calcium channel blocker and α1-adrenergic receptor antagonist used as an antihypertensive. Sugimoto T, Hosoki K ... Karasawa T (July 1995). "Relative contribution of alpha 1-adrenoceptor blocking activity to the hypotensive effect of the novel ... calcium antagonist monatepil". Journal of Cardiovascular Pharmacology. 26 (1): 55-60. doi:10.1097/00005344-199507000-00009. ...
Niguldipine
... is a calcium channel blocker and a1-adrenergic receptor antagonist. Boer R, Grassegger A, Schudt C, Glossmann H ( ... Niguldipine binds with very high affinity to Ca2+ channels and to a subtype of alpha 1-adrenoceptors". European Journal of ...
BMY-7,378
... is a 5-HT1A receptor weak partial agonist/antagonist and α1D-adrenergic receptor antagonist. Goetz AS, King HK, Ward ... "BMY 7378 is a selective antagonist of the D subtype of alpha 1-adrenoceptors". European Journal of Pharmacology. 272 (2-3): R5- ...
Beta-1 adrenergic receptor
Other adrenergic receptors Alpha-1 adrenergic receptor Alpha-2 adrenergic receptor Beta-2 adrenergic receptor Beta-3 adrenergic ... β1-selective antagonists include: Acebutolol (in hypertension, angina pectoris and arrhythmias) Atenolol (in hypertension, ... "GIPC interacts with the beta1-adrenergic receptor and regulates beta1-adrenergic receptor-mediated ERK activation". The Journal ... is a beta-adrenergic receptor, and also denotes the human gene encoding it. It is a G-protein coupled receptor associated with ...
Abanoquil
... is an α1-adrenergic receptor antagonist. Alpha blocker Tham, TC; Guy, S; Shanks, RG; Harron, DW (1992). "Dose-dependent alpha 1 ... antagonist activity of the anti-arrhythmic drug, abanoquil (UK-52,046), without reduction in blood pressure in man". British ...
Ryanodine receptor
Antagonists:Ryanodine locks the RyRs at half-open state at nanomolar concentrations, yet fully closes them at micromolar ... Non-mammalian vertebrates typically express two RyR isoforms, referred to as RyR-alpha and RyR-beta. Many invertebrates, ... Ryanodine receptors are similar to the inositol trisphosphate (IP3) receptor, and stimulated to transport Ca2+ into the cytosol ... It has been shown that calcium release from a number of ryanodine receptors in a ryanodine receptor cluster results in a ...
Hydralazine Versus Labetalol for the Management of Hypertensive Disorders of Pregnancy - Full Text View - ClinicalTrials.gov
Adrenergic beta-Antagonists. Adrenergic Antagonists. Adrenergic Agents. Neurotransmitter Agents. Molecular Mechanisms of ...
https://clinicaltrials.gov/ct2/show/NCT01538875?recr=Open&cond=%22Pregnancy%2C+Ectopic%22&rank=7 Effects of the Use of Adjuvant Drugs After Extracorporeal Shockwave Lithotripsy (ESWL) in Renal Calculus - Full Text View -...
Adrenergic alpha-Antagonists. Adrenergic Antagonists. Adrenergic Agents. Neurotransmitter Agents. Molecular Mechanisms of ... Some drugs, like alpha blockers and calcium channel blockers, can improve the success rates of this procedure. Our objective is ...
https://clinicaltrials.gov/ct2/show/NCT01215708?cond=%22Kidney+Calculi%22&rank=7
Sympatholytic pharmacology Flashcards by Joseph Calderaro | Brainscape
What makes up a mixed adrenergic receptor antagonist? Non-selective B receptor antagonist. alpha 1 receptor antagonist ... The added Beta antagonist will prevent the reflex tachycardia commonly associated with alpha 1 receptor antagonists ... Folklore says that inhibition of a2 adrenergic receptors with Yohimbine treats what? ... Browse over 1 million classes created by top students, professors, publishers, and experts, spanning the world's body of " ...
https://www.brainscape.com/flashcards/sympatholytic-pharmacology-4357844/packs/6409003
Gastric Antral Vascular Ectasia disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials
Adrenergic alpha-Antagonists. 13. Adrenergic Antagonists. 14. Adrenergic beta-Antagonists. 15. Anticholesteremic Agents. ... ATPase H+/K+ Transporting Alpha Subunit. 15.72. DISEASES inferred 14 GeneCards inferred via :. DISEASES inferred (show sections ... The MalaCards human disease database index: 1-9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z ... CST Telomere Replication Complex Component 1. 15.52. DISEASES inferred 14 GeneCards inferred via :. DISEASES inferred (show ...
http://www.malacards.org/card/gastric_antral_vascular_ectasia
Textbook of Psychiatry/Psychopharmacology - Wikibooks, open books for an open world
It is an antagonist at alpha-2-adrenergic autoreceptors thereby increasing norepinephrine and serotonin release, and it blocks ... but may have similar receptor occupancy to the more potent SGAs.(Seeman, 2002) It has alpha-adrenergic antagonism and ... It is similar to FGAs in that it is a potent D2 receptor antagonist, but like many other SGAs, it is also a post-synaptic ... Propranolol is a beta-adrenergic antagonist. Although it is primarily used medically for its effect on heart rate and blood ...
https://en.wikibooks.org/wiki/Textbook_of_Psychiatry/Psychopharmacology![urinary tract neoplasms benign drug therapy 2000:2010[pubdate] *count=100 - BioMedLib™ search engine](data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAABAAAAAQCAIAAACQkWg2AAAAA3NCSVQICAjb4U/gAAABLUlEQVQokWP8//8/AymAiSTVg1SDfmgut0u8RkDG/DVbGRgYpFO6hBI7IHKx7YsYQ+q//fiZMHlzxvRtUA2X7j59v2NerJtVUmgVAwPDs++/3r/6tOP45VfvPy3Zd4Xh+29GBobvv/5+//0X5iQOttnLN6zYe6J9eikDAwPDv38xNhrVy/dOXX8wwkGL4d9/BkZGRkYGRka4H/79U1OUTfNzqqyd9+TZC4b/DFEOBl9//W1ae6wo0J7hx2+IOkYGqA4Wht9/XW3MxISFGN78fPjsJQMj47cfv1cVh735+IWZmYnh7z+G//8ZGBg+/fj98v3nH7//sjBwsjEqeTDwcNT0JVqb6DMwb/73/7+eqiwDA8Opq/cYeNj/MzDwsLPOvf5sXflSBgYGxpGYNAAO23sdtamYqgAAAABJRU5ErkJggg==)
urinary tract neoplasms benign drug therapy 2000:2010[pubdate] *count=100 - BioMedLib™ search engine
MeSH-minor] Adrenergic alpha-Antagonists / therapeutic use. Disease Progression. Enzyme Inhibitors / therapeutic use. Humans. ... Receptors, Adrenergic, alpha-1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; R9PHW59SFN / naftopidil ... MeSH-minor] Adrenergic alpha-Antagonists / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation. Cell Separation. Cyclin ... MeSH-major] Adrenergic alpha-Antagonists / pharmacology. Prostate-Specific Antigen / analysis. Prostatic Hyperplasia / drug ...
http://www.bmlsearch.com/?kwr=urinary+tract+neoplasms+benign+drug+therapy+2000:2010%5Bpubdate%5D&cxts=100&stmp=b1![ChemIDplus - 34661-75-1 - ICMGLRUYEQNHPF-UHFFFAOYSA-N - Urapidil [INN:BAN:JAN] - Similar structures search, synonyms, formulas,...](data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAABAAAAANCAIAAAAv2XlzAAAAA3NCSVQICAjb4U/gAAAAuklEQVQokb2RMQqDQBRE364BqyjaWaSxEzuLXME+5/AsphJbyQE8ipYewMJGDWIpZlMkQQQhsck0/w/Mg4ERSin2SO5KL0BZIgRCEMcAYUhVARgGbbsCDq8TBPQ9loXrEoY4DscjgOch5RYAWBbA5YKUmCan06fDGljc/Q6Q5zweDAN1jVKcz2jaFlAU2DZCEEX4Pk3DOAJ0HUlCmjLPH0L9oCxT0/T+vwO328p+30HXuV6XSuJfS/+uJ45mi2HVzQbeAAAAAElFTkSuQmCC)
ChemIDplus - 34661-75-1 - ICMGLRUYEQNHPF-UHFFFAOYSA-N - Urapidil [INN:BAN:JAN] - Similar structures search, synonyms, formulas,...
34661-75-1 - ICMGLRUYEQNHPF-UHFFFAOYSA-N - Urapidil [INN:BAN:JAN] - Similar structures search, synonyms, formulas, resource ... Adrenergic alpha-Antagonists. *. Adrenergic Antagonists. *. Antihypertensive Agents. *. Cardiovascular Agents. *. Drug / ... 2,4(1H,3H)-Pyrimidinedione, 6-((3-(4-(2-methoxyphenyl)-1-piperazinyl)propyl)amino)-1,3-dimethyl- (9CI) ... 6-((3-(4-(2-Methoxyphenyl)-1-piperazinyl)propyl)amino)-1,3-dimethyl-2,4(1H,3H)-pyrimidinedione ...
https://chem.nlm.nih.gov/chemidplus/rn/34661-75-1![Locke B[au] - PubMed - NCBI](data:image/png;base64,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)
Locke B[au] - PubMed - NCBI
Pseudoallergic conjunctivitis induced by tamsulosin, a selective alpha-1 adrenergic receptor antagonist. ... 1.. An integrated management strategy to prevent outbreaks and eliminate infection pressure of American foulbrood disease in a ... IGF-1 Mediates EphrinB1 Activation in Regulating Tertiary Dentin Formation.. Matsumura S, Quispe-Salcedo A, Schiller CM, Shin ... 2012 Jan;78(1):227-35. doi: 10.1128/AEM.06094-11. Epub 2011 Oct 21. Erratum in: Appl Environ Microbiol. 2012 Mar;78(6):2073. ...
https://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Locke+B%5Bau%5D&dispmax=50
Japanese Chronic Heart Failure - American College of Cardiology
Keywords: Follow-Up Studies, Adrenergic alpha-1 Receptor Antagonists, Carbazoles, Heart Failure, Stroke Volume, Propanolamines ...
http://www.acc.org/latest-in-cardiology/clinical-trials/2010/02/23/19/10/jchfnbsp8212nbsppresented-at-aha-2009
Presented Data Confirm That RAPAFLO(TM) (silodosin) Provides Rapid, Highly Effective, Symptom Relief for Benign Prostatic...
RAPAFLO(TM) maximizes target organ activity by binding with high affinity to the alpha (1A) receptors concentrated in the ... The binding affinity for the alpha (1B) receptors that cause smooth muscle in peripheral vessels is significantly lower, which ... The antagonism of these receptors cause the smooth muscles in these tissues to relax and results in improved urine flow and a ... RAPAFLO(TM) is an effective, uniquely selective alpha-1 adrenergic receptor antagonist. ...
http://www.bio-medicine.org/medicine-news-1/Presented-Data-Confirm-That-RAPAFLO-28TM-29--28silodosin-29-Provides-Rapid--Highly-Effective--Symptom-Relief-for-Benign-Prostatic-Hyperplasia--28BPH-2-43903-1/ A Category Names List - Drug Information Portal - U.S. National Library of Medicine
Adrenergic alpha-2 Receptor Antagonists (5) • Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS. MeSH ... Adrenergic alpha-Antagonists (65) • Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the ... Adrenergic alpha-2 Receptor Agonists (20) • Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS. MeSH ... Adrenergic Antagonists (132) • Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the ...
https://druginfo.nlm.nih.gov/drugportal/drug/categories A Category Names List - Drug Information Portal - U.S. National Library of Medicine
Adrenergic alpha-2 Receptor Antagonists (5) • Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS. MeSH ... Adrenergic alpha-Antagonists (65) • Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the ... Adrenergic alpha-2 Receptor Agonists (20) • Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS. MeSH ... Adrenergic Antagonists (132) • Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the ...
https://druginfo.nlm.nih.gov/drugportal/jsp/drugportal/drugNamesAndCategories.jsp
New Published Data Demonstrate Long-Term Safety, Efficacy and Tolerability of Watson's RAPAFLO(R) (silodosin) for Benign...
The binding affinity for the alpha (1B) receptors that are in the smooth muscle in peripheral vessels is significantly lower, ... There is moderate affinity to alpha (1D) receptors which are located in the bladder, spinal cord, and nasal passages and ... RAPAFLO(R) maximizes target organ activity by binding with high affinity to the alpha (1A) receptors concentrated in the ... First-generation alpha blockers are nonselective with regard to alpha 1 adrenoreceptor subtypes and, as a result, have been ...
https://www.allergan.com/investors/news/thomson-reuters/new-published-data-demonstrate-long-term-safety-ef
Effects of carvedilol and propranolol on circulatory regulation and oxygenation in cirrhosis - Danish National Research...
Adrenergic alpha-1 Receptor Antagonists; Adrenergic beta-Antagonists; Arteries; Blood Pressure; Blood Volume; Carbazoles; ... BACKGROUND AND AIMS: Newer studies suggest that carvedilol, a beta-blocker with a moderate anti-alpha-1 activity, is superior ... AIMS: to assess potential differential effects of beta-blockers and beta-blockers with moderate anti-alpha-1 activity on ...
http://www.forskningsdatabasen.dk/catalog/256276922
alfuzosin
ANTAGONIST. Ki. 8.55. CHEMBL. CHEMBL. Alpha-1A adrenergic receptor. GPCR. ADA1A_BOVIN ... Alpha-adrenoreceptor antagonists. ATC. G04CA51. GENITO URINARY SYSTEM AND SEX HORMONES. UROLOGICALS. DRUGS USED IN BENIGN ... Alfuzosin is a selective antagonist of post-synaptic alpha1-adrenoreceptors, which are located in the prostate, bladder base, ... 1. 31722-302. TABLET. 10 mg. ORAL. ANDA. 17 sections Alfuzosin Hydrochloride. HUMAN PRESCRIPTION DRUG LABEL. 1. 33261-994. ...
http://drugcentral.org/drugcard/115/view
Thioridazine Drug: Indication, Dosage, Precaution, Side Effect , Storage, Category Type and corresponding Brands - www...
Adrenergic alpha-1 Receptor Antagonists * Cytochrome P-450 CYP1A2 Inhibitors * Cytochrome P-450 CYP1A2 Inducers ...
http://www.genericdrugscan.com/generic/thioridazine Combat Disorder disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials
Adrenergic alpha-Antagonists. Phase 1, Phase 2,Not Applicable. 31. Adrenergic Antagonists. Phase 1, Phase 2,Not Applicable. ... Atypical Chemokine Receptor 1 (Duffy Blood Group). Protein Coding. 15.34. DISEASES inferred 15 ... or (-)-N-Methyl-3-phenyl-3-((alpha,alpha,alpha-trifluoro-p-tolyl)oxy)propylamine ... N-Methyl-3-phenyl-3-((alpha,alpha,alpha-trifluoro-p-tolyl)oxy)propylamine ...
https://www.malacards.org/card/combat_disorder
Relationship between Voided Urine Volume and Urinary ATP in Healthy Volunteers
The strength of the desire to void was classified (none, slight, moderate, or strong; scored from 1 to 4, respectively) and a ... while this increase in urinary ATP was blocked by adrenergic alpha-1 receptor antagonists or anti-muscarinic agents [7] [8] . ... Altered Urinary Bladder Function in Mice Lacking the Vanilloid Receptor TRPV1. Nature Neuroscience, 5, 856-860. https://doi.org ... Moreover, improvement of LUTS in patients with BPH or OAB by treatment with an alpha-1 receptor antagonist or anti-muscarinic ...
https://www.scirp.org/journal/PaperInformation.aspx?PaperID=87819 Poisons and Toxins
Alpha-adrenergic receptor antagonists are antidotal.. Atiparnizole administered at 50 mcg/kg IM reverses signs within 10 ... Mechanism of action Amitraz acts at alpha 2- adrenergic receptor sites in the CNS and at both alphal and alpha 2-adrenergic ... The action produced by each compound depends on the adrenergic receptor or receptors that are activated. Phenylpropanolamine ... adrenergic agonists though phenylpropanolamine also produces mild beta, -adrenergic receptor stimulation and acts indirectly by ...
http://maxshouse.com/Poisons.html Bunazosin - Wikipedia
Systemic Alpha-1 adrenergic receptor antagonists have been implicated in Intraoperative Floppy Iris Syndrome (IFIS). Bunazosin ... Bunazosin (INN) is an alpha 1 antagonist. Bunazosin was initially developed to treat benign prostatic hyperplasia (BPH). It has ...
https://en.wikipedia.org/wiki/Bunazosin
- (EN) This invention relates to certain novel compounds and derivatives thereof, their synthesis, and their use as selective alpha 1a adrenergic receptor antagonists. (wipo.int)
- We have found that (R) alpha-methylhistamine, the selective histamine H3-receptor agonist, attenuates the inotropic and chronotropic response of isolated guinea pig atria to transmural stimulation of adrenergic nerve endings. (aspetjournals.org)
- Abstract OBJECTIVE: By considering the role of adrenergic nervous system in sweat secretion, we postulated that terazosin may be able to improve sweating after taking sertraline, a selective serotonin reuptake inhibitor (SSRI) drug. (ac.ir)
- L-765,314 is a drug which acts as a potent and selective antagonist for the Alpha-1 adrenergic receptor subtype α1B. (medkoo.com)
- 6: Yang XP, Chiba S. Effects of L-765,314, a selective and potent alpha 1B-adrenoceptor antagonist, on periarterial nerve electrical stimulation-induced double-peaked constrictor responses in isolated dog splenic arteries. (medkoo.com)
- Histamine H3-receptor signaling in the heart: possible involvement of Gi/Go proteins and N-type Ca++ channels. (aspetjournals.org)
- Discovered as inhibitory autoreceptors in central histaminergic pathways, histamine H3-receptors may also modulate peripheral cholinergic and central adrenergic function. (aspetjournals.org)
- Our findings indicate that prejunctional histamine H3-receptors modulate the depolarization-dependent norepinephrine release from sympathetic nerve endings in the guinea pig myocardium. (aspetjournals.org)
- We have previously reported that sympathetic stimulation elicits a frequency-dependent release of cardiac histamine, whereas others had found that adrenergic activity regulates histamine's rapid turnover pool. (aspetjournals.org)
- [1] Clozapine is a partial 5-HT1A agonist, contributing to the reduction of negative symptoms and extrapyramidal symptoms, and a muscarinic M1, M2, M3, M5, histamine, and alpha-1 adrenergic-receptor antagonist. (statpearls.com)
- Analysis of the ligand binding properties of RA42 expressed in COS-7 cells with a variety of adrenergic ligands demonstrates a unique alpha 1-adrenergic receptor pharmacology. (nih.gov)
- Tiodazosin is a potent competitive postsynaptic alpha adrenergic receptor antagonist. (medchemexpress.com)
- In vitro comparison of the pre- and postsynaptic alpha adrenergic receptor blocking properties of prazosin and tiodazosin (BL5111). (medchemexpress.com)
- Nicergoline acts by inhibiting the postsynaptic alpha(1)-adrenoceptors on vascular smooth muscle. (drugbank.ca)
- Benzodiazepine receptor agonists directly affect the sleep-wake state-switching system. (medicalmagister.com)
- This is based on a stereospecific binding to a specific recognition site located on the benzodiazepine receptor (GABA A -benzodiazepine receptor complex). (medicalmagister.com)
- Recently, H3-receptors were reported to inhibit adrenergic inotropic responses in guinea pig atria, possibly at prejunctional sites. (aspetjournals.org)
- The antinausea and antiemetic effects of this agent appear to be due to the blockade of 5-HT2 and 5-HT3 receptors for serotonin. (fpnotebook.com)
- As an atypical antipsychotic, clozapine acts an antagonist to both dopamine and serotonin receptors. (statpearls.com)
- The metabolism of Nicergoline can be decreased when combined with 1-(2-Phenylethyl)-4-phenyl-4-acetoxypiperidine. (drugbank.ca)
- [1] Concurrent studies in the United States led to reports of death due to cases of agranulocytosis, taking clozapine off the market for a long time. (statpearls.com)
- [1] A pivotal study known as the US Clozaril Study showed the efficacy of clozapine over chlorpromazine in a 6-week trial of patients who failed to respond to 3 previous antipsychotic drugs. (statpearls.com)
- [1] Norclozapine, the metabolite of clozapine, actively works on the M1 and M4 receptors. (statpearls.com)
- The risk of developing agranulocytosis is around 1% in patients who take clozapine, and this may be independent of dosing. (statpearls.com)
- [1] The definition of treatment-resistant schizophrenia is persistent or moderate delusions or hallucinations after failing 2 trials of antipsychotic medicines. (statpearls.com)
- [1] Antipsychotic drugs are key in treating the core symptoms of schizophrenia: hallucinations and delusions. (statpearls.com)
- It is a type of antipsychotic and a type of monoamine antagonist. (fpnotebook.com)
- Functional characterization of alpha-adrenoceptors mediating pupillary dilation in rats. (medkoo.com)
- Expression of mRNA for this receptor is strongly detected in liver followed by heart, cerebral cortex, brain stem, kidney, lung, and spleen. (nih.gov)
- The present further provides pharmaceutical compositions comprising a somatostatin antagonist and a pharmaceutically acceptable liver targeting compound. (freepatentsonline.com)
- 23. A pharmaceutical composition comprising a somatostatin receptor antagonist and a pharmaceutically acceptable liver targeting substance. (freepatentsonline.com)
- 1.[Detection and identification of major metabolites of clorprenaline in swine urine using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry]. (bocsci.com)
- 2) attenuated by pertussis-toxin pretreatment and 3) potentiated by the N-type Ca(++)-channel blocker omega-conotoxin, which also potentiated the sympathetic modulatory effects of adrenergic-alpha 2 and adenosine-A1 receptor agonists. (aspetjournals.org)
- Melatonin and melatonin receptor agonists influence the "wake signal" from the circadian timing system through their effects on MT 1 and MT 2 receptors. (medicalmagister.com)
- Alpha-1 subunit mediates both sedation and memory effects of agonists. (medicalmagister.com)
- 2016 Feb 1;192:188-96. (bocsci.com)
- 1. A method of treating HISS-dependent insulin resistance comprising administering a therapeutically effective amount of a somatostatin antagonist to a patient in need thereof. (freepatentsonline.com)
- 9. The method according to claim 1, wherein the somatostatin antagonist is selected from the group consisting of DC-41 -33, BIM-23454, SB-710411, cyclo (7-aminoheptanoyl-Phe-D-Trp-Lys-O-benzyl-Thr), AC-178,335 and a combination thereof. (freepatentsonline.com)
- Accordingly, presynaptic H3-receptors are likely to serve a modulatory role in cardiac adrenergic function. (aspetjournals.org)
- It has mainly been used to investigate the role of α1B receptors in the regulation of blood pressure. (medkoo.com)
- OBJECTIVES:1) To compare efficacy and severe persistent hypertension after intravenous Labetalol versus Hydralazine, within maximum 5 drug boluses, in obstetric severe hypertensive patients at Civil Hospital Karachi. (clinicaltrials.gov)
- The primary structure though most closely resembles that of an alpha 1-adrenergic receptor, having approximately 73% amino acid identity in the putative transmembrane domains with the previously isolated hamster alpha 1B receptor. (nih.gov)
- Pharmacological and molecular cloning studies have demonstrated heterogeneity of alpha 1-adrenergic receptors. (nih.gov)
- There are two particular combinations of isoforms that are noted Type-I (alpha 1, beta 2, gamma 2) and Type-II (alpha 3, beta 2, gamma 2) configurations. (medicalmagister.com)
- Type-1 configuration is the most common type representing roughly 40% of GABA A receptors. (medicalmagister.com)
- Zolpidem and Zaleplon bind with relatively greater specificity to the Type-I receptor. (medicalmagister.com)
- Evidence that alpha(1B)-adrenoceptors are involved in noradrenaline-induced contractions of rat tail artery. (medkoo.com)
- Subjects' hand will be submerged in cold water (~0-1°C) up to the wrist for 1 minute. (clinicaltrials.gov)
- The risk or severity of hypertension can be increased when Nicergoline is combined with 1-(3-Mercapto-2-Methyl-Propionyl)-Pyrrolidine-2-Carboxylic Acid. (drugbank.ca)
- The risk or severity of hypertension can be increased when Nicergoline is combined with 1-benzylimidazole. (drugbank.ca)
- Northern blot analysis of various rat tissues also shows the distribution expected of the alpha 1A receptor subtype with abundant expression in vas deferens followed by hippocampus, cerebral cortex, aorta, brainstem, heart and spleen. (nih.gov)
- For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER. (cigna.com)
- The actual binding site for benzodiazepines is located at the junction of the alpha and gamma subunits. (medicalmagister.com)
- It is most frequently related to the use of anticholinergics drugs [1, (bittnerdentalclinic.com)