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Propranolol

Propranolol is a non-selective beta-adrenergic receptor antagonist used to treat a variety of cardiovascular conditions, including hypertension, angina pectoris, and certain cardiac arrhythmias.
It may also be used to manage essential tremor and migraine headaches.
Propranolol works by blocking the effects of the hormone epinephrine, which normally binds to and activates beta-adrenergic receptors, leading to increased heart rate, blood pressure, and other physiological effects.
By antagonizing these receptors, propranolol reduces the cardiovascular strain associated with sympathetic nervous system activation.
Researches can utilize PubCompare.ai to optimize their propranolol studies, locating and compareing the most accurate and reproducable research methods across published literature, preprints, and patents.

Most cited protocols related to «Propranolol»

Clozapine was provided as a generous gift to J.H.P. from Novartis (Hanover, NJ, USA). Olanzapine was provided as a generous gift to J.H.P. from Eli Lilly (Indianapolis, IN, USA). Clozapine, olanzapine, and risperidone were supplied to D.W. by the National Institute of Mental Health’s Chemical Synthesis and Drug Supply Program. Haloperidol, prazosin, propranolol, and ritanserin were purchased from Sigma-Aldrich (St. Louis, MO, USA). J.H.P. and M.S.F. obtained CNO from the Rapid Access to Investigative Drug Program funded by the National Institute of Neurological Disorders and Stroke. D.W. obtained CNO from the National Institute on Drug Abuse Drug Supply Program.
Clozapine, olanzapine, risperidone, haloperidol, prazosin, propranolol, and ritanserin were each dissolved in distilled water with 2–3 drops of lactic acid and pH-adjusted to 6.0–7.0 with NaOH. For mouse drug discrimination studies, CNO was also dissolved in this vehicle. For rat drug discrimination studies and for mouse and rat pharmacokinetic analyses, CNO was dissolved in bacteriostatic saline containing v/v 2.5–5.0% dimethyl sulfoxide (Sigma-Aldrich) and 10% Cremophor EL (Sigma-Aldrich).
For mouse drug discrimination studies, all drugs were administered s.c. at a volume of 10 ml/kg, 30 min prior to session onset. For rat drug discrimination studies, all drugs were administered i.p. at a volume of 1 ml/kg. Clozapine was administered 60 min prior to session onset, while olanzapine, risperidone, prazosin, and propranolol were administered 30 min prior to session onset. CNO was tested at both 30 and 60 min pretreatment times. All drug doses are expressed as the salt weight.
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Publication 2018
Anabolism Clozapine cremophor EL Discrimination, Psychology Haloperidol Lactic Acid Mice, House Olanzapine Pharmaceutical Preparations Prazosin Propranolol Risperidone Ritanserin Saline Solution Sodium Chloride Sulfoxide, Dimethyl
A 3-lead ECG was recorded from male volunteers aged 18 to 30 years: 8 competitive endurance athletes and 10 sedentary age-matched (control) subjects. The heart rate was measured before and after complete autonomic blockade (achieved by intravenous injection of 0.04 mg/kg atropine and 0.2 mg/kg propranolol followed by top-up doses). After complete autonomic blockade, 7.5 mg ivabradine was administered orally, and the change in heart rate was recorded and used as a measure of the involvement of If in pacemaking. Ten-week-old C57BL/6J mice were trained by swimming for 60 minutes twice daily for 28 days.5 (link) miR, mRNA, and protein expression in sinus node biopsies was measured by next-generation sequencing, quantitative real-time reverse transcription polymerase chain reaction (qPCR), Western blot, and high-resolution mass spectrometry. Computational predictions, luciferase reporter gene assays, and in vitro overexpression studies were used to identify miRs and transcription factors capable of regulating expression. The role of a candidate miR in the training-induced bradycardia was tested in vivo by administering an appropriate cholesterol-conjugated anti-miR.6 (link) ECG recording, in vitro tissue electrophysiology, Western blot, sinus node cell isolation, and whole-cell patch clamp were used to characterize the mice and study HCN4 and If remodeling. Statistically significant differences were determined using an appropriate test; P<0.05 was regarded as significant. In figures, bar charts show means±SEM. Further details of methods are available in the Online Data Supplement.
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Publication 2017
Antagomirs Athletes Atropine Autonomic Nerve Block Biological Assay Biopsy Cells Cell Separation Cholesterol Dietary Supplements Genes, Reporter Ivabradine Luciferases Males Mass Spectrometry Mice, Inbred C57BL Mus Propranolol Proteins Rate, Heart Real-Time Polymerase Chain Reaction Reverse Transcription RNA, Messenger Sinoatrial Node Tissues Transcription Factor Voluntary Workers Western Blot
For a full description of the Materials and Methods see the Supplemental Information. Briefly, fifty-four healthy young human participants were initially included in the study. In a double-blind design, participants were pseudo-randomly assigned to one of the drug groups so that for each of four consecutive participants two would receive a beta-blocker (40mg Propranolol HGl) and two placebo (microcrystalline cellulose). Five participants were excluded on Day 1 as they displayed no conditioned skin conductance responses, three participants could not complete the study due to scanner problems and one participant in the propranolol group did not complete the reinstatement and re-extinction task due to scanner problems. The placebo group comprised 24 participants (11 males, 13 females) and the propranolol group 22 participants (8 males, 14 females). All participants gave written informed consent. The study was approved by the institutional ethics committee (CMO Regio Arnhem-Nijmegen, The Netherlands, CMO2010/257).
Over three consecutive days participants were differentially cue-conditioned to a stimulus signaling threat (CS+) of transcutaneous electrical shock (US) and a cue signaling safety (CS−) in a specific context on Day 1 (Fig. S1a). On Day 2 participants received a single dose of propranolol or placebo and underwent an extinction paradigm. On Day 3, in the absence of drug, the possible return of fear was first tested as spontaneous recovery during a recall task. Next, a stronger test of fear recovery was employed where first the general level of arousal was increased by four unsignaled shocks, and next fear reinstatement was assessed during a re-extinction task. The context of extinction, recall, and re-extinction differed from conditioning (ABBB design) to better match treatment settings, and to maximize the chance of detecting hippocampal responses (Kalisch et al, 2006 (link); Marschner et al, 2008 (link); Milad et al, 2007 (link)). We measured the influence of beta-blocker administration on Day 2 on (a) learned fear as indexed by skin conductance responses (SCR) (Bach et al, 2011 (link)) on Day 2 and 3, (b) explicit memory and subjective experience of the fearful events tested at the end of Day 3, (c) neural functioning using Blood Oxygenation Level Dependent functional Magnetic Resonance Imaging (BOLD-fMRI) on Day 2 and 3, (d) the relationship between behavior (SCR and explicit memory) and neural responses, and (e) a neural signature of reinforcement learning.
Publication 2015
Adrenergic beta-Antagonists Arousal BLOOD Cell Respiration Conditioned Reflex Electricity Extinction, Psychological Fear Females Healthy Volunteers Homo sapiens Institutional Ethics Committees Males Memory Mental Recall microcrystalline cellulose Nervousness Pharmaceutical Preparations Placebos Propranolol Reinforcement, Psychological Safety Shock Skin
We modeled participants’ behavior using maximum likelihood estimation as implemented in MATLAB (Mathworks, Natick, MA) to fit a prospect-theory-inspired model (Tversky & Kahneman, 1992 (link)) to choices, identical to that used in previous studies (Sokol-Hessner, et al., 2013 (link); Sokol-Hessner, et al., 2014 (link); Sokol-Hessner, et al., 2009 (link)).
u(x+)=p×(x+)ρ
u(x)=λ×p×(x)ρ
p(gamble)=11+eμ×(u(gamble)u(guaranteed))
Equations 1 and 2 calculate the utility of gains and losses respectively. These are used to compute the utility of the gamble and the guaranteed alternative, which are then converted into a probability of choosing the gamble using the softmax in Equation 3. The model’s parameters quantify loss aversion (λ, the relative multiplicative weight placed on losses compared to gains), risk attitudes (ρ, feelings about chance/diminishing marginal sensitivity to value), and choice consistency (μ, noisiness in choices, also called the softmax temperature). All analyses of loss aversion used log(λ); the logarithm is commonly used since λ is positively skewed.
This task has the ability to separate changes in loss aversion from those in risk attitudes by including both gain-loss and gain-only trial types. Gain-loss trials consist of a gamble with positive and negative possible outcomes, and a guaranteed alternative of zero. Choices in these trials reflect both risk attitudes (because the gamble is risky) and loss aversion (because losses are being evaluated). Gain-only trials consist of a gamble with possible outcomes of a large positive amount or zero, and a guaranteed alternative of a small positive amount. In these trials, risk attitudes affect behavior (because the gamble is still risky), but loss aversion does not (because there are no losses). When gain-loss and gain-only trials are simultaneously fit, risk attitudes are estimated that account for behavior across all trials, while loss aversion accounts for the remainder of gain-loss gambling behavior not explained by risk attitudes. In studies that only include gain-loss trial types, it is impossible to identify to what extent loss aversion or risk aversion is driving behavior because both processes are present and have similar gross effects on behavior (increasing or decreasing gambling). Both gain-loss and gain-only trial types are necessary to separately identify risk attitudes and loss aversion.
To analyze changes in choice behavior, we first regressed the change in log(λ) across days on Day (the constant), Medication (−1 placebo to propranolol; +1 propranolol to placebo), BMI group (+1 Low BMI group; −1 High BMI group), and the interaction between Medication and BMI group. We also did this exact regression using risk attitudes (ρ) and choice consistency (μ) instead of log(λ). To clarify the effect of the interaction, we subtracted the strong Day effect from the change in log(λ) leaving the residual change in loss aversion (ΔλR) due to propranolol. The resulting values were still in “Day” space (i.e. reflecting changes from Day 1 to Day 2), so we flipped the sign of the values corresponding to individuals who received placebo on Day 1 so that all values were in a “Medication” space (reflecting propranolol-to-placebo changes). We called this ΔλR as it reflected the residual change in loss aversion due to propranolol, and performed subsequent analyses on these residuals.
We think it likely that there is some more continuous relationship between BMI and a constant 80mg dose of propranolol. However, this relationship is certainly non-linear, characterized by both ceiling effects (in which 80mg of propranolol has a constant, maximal effect below some BMI) and floor effects (in which 80 mg of propranolol has no observable effect above a particular BMI). To avoid arbitrary assumptions of functional forms, and allow our data to shape the monotonic transformation of BMI, we used nonlinear curve fitting procedures in MATLAB (NonLinearModel.fit) to fit a model based on the following two equations:
tBMI=z(11+eα+γ×z(BMI))
log(λDay2)log(λDay1)=β1×Day+β2×Medication+β2×tBMI+β4×Medication×tBMI in which z() indicates the use of z-scoring. This regression is identical to that described earlier, except instead of a median split on BMI, we allowed the modified softmax function (Equation 4, parameterized by α and γ) to transform BMI into tBMI as best fit the change in loss aversion. This transformation function avoids arbitrary assumptions as it can approximate a wide variety of possible monotonic relationships including linear, sigmoidal, curvilinear, or step functions, and is thus capable of modeling both ceiling and floor effects. For analyses using BMI as a strictly linear covariate, see Supplementary Materials, though note non-linearity caveats above.
Publication 2015
Feelings Pharmaceutical Preparations Placebos Propranolol

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Publication 2015
Animals BLOOD Lung Propranolol Rattus norvegicus Shock, Hemorrhagic

Most recents protocols related to «Propranolol»

Example 5

In order to compare levels of adherence to HEp-2 epithelial cells in culture, we used an established model for evaluating adherence of EHEC O157:H7 (27). HEp-2, human laryngeal carcinoma epithelial cells, were a kind gift from Dr. Carlton Gyles (Department of Pathobiology, University of Guelph). Briefly, HEp-2 cells grown in EMEM supplemented with 10% (v/v) FBS were plated onto 24-well tissue culture plates at 2×105 cells ml−1 and incubated for 24 h in the presence of 5% CO2. The cells were then maintained during the assay in serum and antibiotic-free EMEM. Before inoculation with bacteria, 10% (v/v) of L. acidophilus CFSM selected fractions were added in triplicate to treatment group wells. Wells containing the negative control groups were inoculated with 105 E. coli O157:H7 strain VS94 with or without supplementation with 100 μM propanolol (Sigma-Aldrich Canada Ltd.). Following inoculation of 105 EHEC O157 into treatment and control group wells, the plates were incubated for 3 h at 37° C. in the presence of 5% CO2. The cell monolayers were then washed three times with PBS to remove non-adhering bacteria and fresh medium was added. Cells were incubated for another 3 h and then washed six times with PBS. Washed cells were lysed with 0.1% Triton X-100. Released bacteria present in the suspension were collected and appropriate dilutions were plated on LB agar. To evaluate if the percentage of adherence in the treatment groups was significantly different from that of the control group, where the recovered counts from the control group (2.2×107 CFU ml−1) were considered to be 100%, the percentage of adherence in the negative control and treatment groups were calculated using the following equation.

% of Recovery = Group _ 2.2 × 10 7 CFU ml - 1 × 100 _

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Patent 2024
Agar Antibiotics Bacteria Bacterial Vaccines Biological Assay Carcinoma Cell Adhesion Cell Culture Techniques Cells Enterohemorrhagic Escherichia coli Epithelial Cells Escherichia coli O157 Homo sapiens Lactobacillus acidophilus Larynx Propranolol Serum Strains Technique, Dilution Tissues Triton X-100 Vaccination
We retrospectively collected demographic data (age, sex, height, and weight), medical history (psychiatric, gastrointestinal, vascular, hormonal, cancer, respiratory, and immuno-rheumatologic), and the following headache characteristics: onset age, family history of headache, migraine characteristics (unilateral pain, pulsating pain, or aggravation by routine physical activity), pain intensity (0–10; numerical rating scale [NRS]), associated symptoms (photophobia, phonophobia, and nausea/vomiting; none, mild, moderate, or severe), and the presence of aura. The headache specialist explained the criteria for migraine based on the ICHD-3 to all patients who were asked to track headache and migraine days (including probable migraine days). Patients completed a questionnaire on monthly migraine days (MMD), monthly headache days (MHD), monthly acute medication intake days (AMD) at baseline and MMD after 3 months of treatment. A month was defined as 28 days. The headache specialist verified the accuracy and reliability of the completed questionnaire by interviewing and occasionally reviewing each patient’s headache diary. Patients were classified as having episodic migraine or chronic migraine, according to the ICHD-3. Patients were also diagnosed with MOH based on the ICHD-3. Patients completed the Generalized Anxiety Disorder-7 (GAD-7) questionnaire [27 (link), 28 ] and Patient Health Questionnaire-9 (PHQ-9) [29 (link)] upon CGRPmAb administration to determine the extent of anxiety and depression, respectively. We also collected patient migraine-preventive drug data, including failures of preventative drugs (lomerizine, propranolol, valproate, amitriptyline, or topiramate) before CGRPmAb treatment and response frequency to triptan (0, 1, 2, 3 out of three uses) [10 (link)].
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Publication 2023
Amitriptyline Anxiety Headache Hematologic Neoplasms lomerizine Migraine Disorders Nausea Pain Patients Pharmaceutical Preparations Phonophobia Photophobia Propranolol Respiratory Rate Severity, Pain Topiramate Triptans Valproate
The collection time of the plasma sample included data from before administration of bepridil to up to 6 h after administration. To assess risk factors for achieving plasma bepridil concentrations ≥800 ng/mL at steady state, the eligible patients were divided into two groups based on their bepridil concentrations: ≥800 ng/mL and < 800 ng/mL.
The C/D ratio was calculated using the following equation:
C/D ratio of bepridil = plasma concentration of bepridil (ng/mL) / dose of bepridil (mg/day/kg body weight).
In this study, we defined the polypharmacy group as those who use six or more drugs, whereas the non-polypharmacy group was those who took fewer than six drugs. The relationship between plasma bepridil concentrations ≥800 ng/mL and baseline characteristics, including sex, age, height, body weight, body mass index, serum creatinine, creatinine clearance (Ccr), number of concomitant drugs used, typical inducers of CYPs (phenytoin, carbamazepine, phenobarbital, and rifampicin) [15 (link)], typical inhibitors of CYPs (erythromycin, clarithromycin, protease inhibitors, and azole antifungals) [15 (link)], aprindine, a competitive inhibitor of CYP2D6 [12 (link)], typical inhibitor of P-gp (amiodarone, diltiazem, nicardipine, nifedipine, propranolol, quinidine, cyclosporin, and tacrolimus) [16 (link)–18 (link)], and left ventricular ejection fraction (LVEF), were examined. LVEF was measured using echocardiographic equipment provided at each hospital. Ccr was estimated using the Cockcroft–Gault formula [19 (link)].
The patient’s medical history and duration of bepridil treatment were collected from medical records.
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Publication 2023
Amiodarone Antifungal Agents Aprindine Azoles Bepridil Body Weight Carbamazepine Clarithromycin Creatinine Cyclosporine Cytochrome P-450 CYP2D6 Inhibitors Cytochrome P450 Diltiazem Echocardiography Erythromycin Index, Body Mass inhibitors Nicardipine Nifedipine Patients Pharmaceutical Preparations Phenobarbital Phenytoin Plasma Polypharmacy Propranolol Protease Inhibitors Quinidine Rifampin Serum Specimen Collection Tacrolimus Ventricular Ejection Fraction

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Publication 2023
Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Anti-Anxiety Agents Antiepileptic Agents Antipsychotic Agents Anxiety Aripiprazole Ativan Benadryl Benzodiazepines brexanolone Buspar Care, Ambulatory Clonazepam Depression, Postpartum Desvenlafaxine Dopamine Uptake Inhibitors Duloxetine Escitalopram Ethics Committees, Research Ethnicity Fluoxetine Hispanics Histamine H1 Antagonists Lithium Lurasidone Mood Norepinephrine Obstetric Delivery Olanzapine Patients Post-Traumatic Stress Disorder Prazosin Pregabalin Propranolol Psychotropic Drugs Quetiapine Selective Serotonin Reuptake Inhibitors Serotonin Uptake Inhibitors Sertraline SNRIs Trazodone Treatment Protocols Vistaril Wellbutrin Woman
This cross-sectional study was performed in 2021 at Khorshid Hospital, affiliated with Isfahan University of Medical Sciences. The records of all patients who were referred to our center in 2018 because of beta-blocker poisoning were reviewed. The study protocol was approved by the Research Committee of Isfahan University of Medical Sciences, and the Ethics Committee confirmed it (IR.MUI.MED.REC.1399.040).
The inclusion criteria were the age of more than 8 years, poisoning by beta-blockers, availability of medical records, and complete medical documents. Among 259 patients who were suspected of beta-blocker intoxication, 255 were included in the study. In multiple drug intakes, patients who had taken cardiovascular drugs (antihypertensive andantiarrhythmic) with beta-blockers were excluded from the study. Patients with a history of severe cardiac arrhythmia, renal and hepatic dysfunction, and those who left the hospital voluntarily or without permission while their follow-up was continuing were excluded. Patients were categorized into three groups according to the type of drug poisoning as propranolol, other beta-blockers (including metoprolol, bisoprolol, atenolol, and carvedilol), and the combination of beta-blockers, respectively (Figure 1).
The following information about poisoning was collected from the documents: personal characteristics (such as age, sex, marital status, level of education, and occupation), characteristics related to poisoning (type of drug, number of drug taken, and location of drug use), and mode of poisoning (intentional, accidental, and overdose), history of addiction and type of addiction (alcohol, cigarettes, opiates, or others), length of hospitalization, medical history related to psychiatric illness, and suicide history, as well as clinical findings in main organs including the central nervous system (CNS), heart, skin, eye (miosis or mydriasis), deep tendon reflex, palmar reflex, and vital signs (blood pressure, respiration rate, pulse rate, and body temperature) at baseline, laboratory data, treatments performed (receiving charcoal, atropine, glucose, calcium glucagon, dialysis) and other treatments, and treatment outcome (complete recovery or death). All poisonings registered in our medical center were collected after extracting the desired data and entering them into a computer file with a special format.
The obtained data were entered into the Statistical Package for Social Sciences (SPSS) version 24. Statistical analyzes were performed in two parts: descriptive and analytical. In the descriptive part, the reports were presented in the form of a percentage (number) for qualitative variables and an average (variance) for quantitative variables. In the analytical section, the relationship between age, sex, frequency of predictive factors, and outcome therapy was examined based on different outcomes by eliminating possible confounders using logistic regression. We used independent t-tests and repeated measure tests to compare data between different timelines and different groups. P < 0.05 was considered statistically significant.
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Publication 2023
Accidents Addictive Behavior Adrenergic beta-Antagonists Antihypertensive Agents Arecaceae Atenolol Atropine Bisoprolol Blood Pressure Body Temperature Calcium Cardiac Conduction System Disease Cardiovascular Agents Carvedilol Central Nervous System Charcoal Dialysis Drug Overdose Ethanol Ethics Committees Glucagon Glucose Heart Hospitalization Kidney Mental Disorders Metoprolol Mydriasis Opiate Alkaloids Patients Pharmaceutical Preparations Poisoning Propranolol Pulse Rate Pupils, Constricted Reflex Reflex, Tendon Respiratory Rate Signs, Vital Signs and Symptoms Skin Therapeutics TimeLine

Top products related to «Propranolol»

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Propranolol is a laboratory reagent used as a β-adrenergic receptor antagonist. It is commonly used in research applications to study the role of the sympathetic nervous system.
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Propranolol hydrochloride is a pharmaceutical compound that functions as a beta-adrenergic blocking agent. It is commonly used in the production and testing of various pharmaceutical and medical products.
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Propranolol is a laboratory reagent used in various research applications. It is a beta-blocker that acts as a non-selective antagonist for beta-adrenergic receptors. This product is intended for research use only and not for use in diagnostic procedures.
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Isoproterenol is a synthetic catecholamine used as a laboratory reagent. It acts as a non-selective beta-adrenergic agonist, stimulating both beta-1 and beta-2 adrenergic receptors. Isoproterenol is commonly used in research applications to study cardiovascular and respiratory function.
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Atenolol is a laboratory equipment product developed by Merck Group. It functions as a beta-blocker, a class of medications used to regulate heart rate and blood pressure. The core function of Atenolol is to manage cardiovascular conditions by controlling the body's response to certain hormones.
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Prazosin is a laboratory equipment product manufactured by Merck Group. It is a chemical compound used in research and scientific applications. Prazosin is primarily used as a standard reference material and a research tool in various scientific fields.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Methanol is a clear, colorless, and flammable liquid that is widely used in various industrial and laboratory applications. It serves as a solvent, fuel, and chemical intermediate. Methanol has a simple chemical formula of CH3OH and a boiling point of 64.7°C. It is a versatile compound that is widely used in the production of other chemicals, as well as in the fuel industry.
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Norepinephrine is a laboratory product produced by Merck Group. It is a neurotransmitter and hormone that plays a role in the sympathetic nervous system. The core function of Norepinephrine is to regulate physiological processes such as heart rate, blood pressure, and pupil dilation.

More about "Propranolol"

Propranolol, a non-selective beta-blocker, is a widely used medication for the treatment of a variety of cardiovascular conditions, including hypertension, angina pectoris, and certain cardiac arrhythmias.
It may also be employed to manage essential tremor and migraine headaches.
Propranolol hydrochloride, the salt form of the drug, shares similar therapeutic properties.
By blocking the effects of the hormone epinephrine (also known as adrenaline), propranolol reduces the cardiovascular strain associated with sympathetic nervous system activation, leading to a decrease in heart rate, blood pressure, and other physiological effects.
Researchers can leverage PubCompare.ai to optimize their propranolol studies, locating and comparing the most accurate and reproducible research methods across published literature, preprints, and patents.
This AI-driven analysis can help identify the most trustworthy and reliable protocols, enhancing the quality and efficacy of propranolol research.
Additionally, the platform can be utilized to explore related compounds, such as Isoproterenol, a synthetic beta-agonist, and Atenolol, another beta-blocker, as well as commonly used experimental reagents like FBS (Fetal Bovine Serum), DMSO (Dimethyl Sulfoxide), Methanol, and Norepinephrine.
By incorporating these insights, researchers can design more robust and informative studies, ultimately advancing our understanding of propranolol and its clinical applications.