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Inderal (Propranolol)

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Inderal is an effective medication which helps to fight with hypertension and other heart or circulatory conditions. It is also taken to prevent heart attack and reduce severe headaches. Inderal acts by affecting the heart and circulation.

Other names for this medication:

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Also known as:  Propranolol.


Inderal is a perfect remedy, which helps to fight against hypertension and other heart or circulatory conditions. Its target is to prevent heart attack and reduce severe headaches.

Inderal acts by affecting the heart and circulation. It is beta blocker.

Inderal is also known as Propranolol, Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Sumial, Anaprilinum.

Generic name of Inderal is Propranolol.

Brand names of Inderal are Inderal, Inderal LA, InnoPran XL.


The dosage of Inderal depends on your condition.

Take Inderal tablets and capsules every day at the same time orally with water.

Do not crush or chew it.

The extended-release (long-acting) tablet is usually taken once a day. Immediate-acting Inderal can be taken 2-4 times a day.

If you want to achieve most effective results do not stop taking Inderal suddenly.


If you overdose Inderal and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Inderal overdosage: shortness of breath, uneven heartbeats, seizure, weakness, fainting, dizziness, bluish-colored fingernails.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Inderal are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Inderal if you are allergic to Inderal components.

Do not take Inderal if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Be careful with Inderal if you are taking heart medicines (such as nifedipine (Procardia, Adalat), reserpine (Serpasil), verapamil (Calan, Verelan, Isoptin), diltiazem (Cartia, Cardizem)), MAO inhibitor (such as isocarboxazid (Marplan), tranylcypromine (Parnate), phenelzine (Nardil), or selegiline (Eldepryl, Emsam)),cold medicines, stimulant medicines or diet pills,medicine for asthma or other breathing disorders (such as albuterol (Ventolin, Proventil), bitolterol (Tornalate), metaproterenol (Alupent), pirbuterol (Maxair), terbutaline (Brethaire, Brethine, Bricanyl) and theophylline (Theo-Dur, Theolair)),a diabetes medication (such as insulin, glyburide (Diabeta, Micronase, Glynase), glipizide (Glucotrol), chlorpropamide (Diabinese), or metformin (Glucophage)), allergy medicine, guanabenz (Wytensin),clonidine (Catapres).

Be careful with Inderal if you suffer from or have a history of bradycardia (<50 beats/minute), uncontrolled congestive heart failure, sick sinus syndrome, atrioventricular block (2 or 3 degree), cocaine toxicity, asthma or chronic obstructive pulmonary disease (COPD), diabetes, depression, liver or kidney disease, myasthenia gravis, Raynaud's syndrome. You can take Inderal on the lower dose.

Be careful with Inderal if you are going to have a surgery.

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Inderal suddenly.

inderal migraine dosage

As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via beta-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the beta-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a +1.5 degrees C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap - TBack) by +1 degrees C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4 degrees C) induced a +2.7 degrees C increase in TiScap-TBack, which was reduced to +1 degrees C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by beta-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either.

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Bone and lung metastases are responsible for the majority of deaths in patients with breast cancer. Following treatment of the primary cancer, emotional and psychosocial factors within this population precipitate time to recurrence and death, however the underlying mechanism(s) remain unclear. Using a mouse model of bone metastasis, we provide experimental evidence that activation of the sympathetic nervous system, which is one of many pathophysiological consequences of severe stress and depression, promotes MDA-231 breast cancer cell colonization of bone via a neurohormonal effect on the host bone marrow stroma. We demonstrate that induction of RANKL expression in bone marrow osteoblasts, following β2AR stimulation, increases the migration of metastatic MDA-231 cells in vitro, independently of SDF1-CXCR4 signaling. We also show that the stimulatory effect of endogenous (chronic stress) or pharmacologic sympathetic activation on breast cancer bone metastasis in vivo can be blocked with the β-blocker propranolol, and by knockdown of RANK expression in MDA-231 cells. These findings indicate that RANKL promotes breast cancer cell metastasis to bone via its pro-migratory effect on breast cancer cells, independently of its effect on bone turnover. The emerging clinical implication, supported by recent epidemiological studies, is that βAR-blockers and drugs interfering with RANKL signaling, such as Denosumab, could increase patient survival if used as adjuvant therapy to inhibit both the early colonization of bone by metastatic breast cancer cells and the initiation of the "vicious cycle" of bone destruction induced by these cells.

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Trimetazidine is an effective and well tolerated anti-ischaemic agent which, in addition to providing symptom relief and functional improvement in patients with angina pectoris, has a cytoprotective action during ischaemia. The drug is suitable for initial use as monotherapy in patients with angina pectoris and, because of its different mechanism of action, as adjunctive therapy in those with symptoms not sufficiently controlled by nitrates, beta-blockers or calcium antagonists. The role of trimetazidine in other coronary conditions has yet to be clearly established.

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The use of fluorescent proteins, particularly when genetically fused to proteins of biological interest, have greatly advanced many flow cytometry research applications. However, there remains a major limitation to this methodology in that only total cellular fluorescence is measured. Commonly used fluorescent proteins (e.g., EGFP and its variants) are fluorescent whether the fusion protein exists on the surface or in sub-cellular compartments. A flow cytometer cannot distinguish between these separate sources of fluorescence. This can be of great concern when using flow cytometry, plate readers or microscopy to quantify cell surface receptors or other surface proteins genetically fused to fluorescent proteins. Recently developed fluorogen activating proteins (FAPs) solve many of these issues by allowing the selective visualization of only those cell surface proteins that are exposed to the extracellular milieu. FAPs are GFP-sized single chain antibodies that specifically bind to and generate fluorescence from otherwise non-fluorescent dyes ('activate the fluorogen'). Like the fluorescent proteins, FAPs can be genetically fused to proteins of interest. When exogenously added fluorogens bind FAPs, fluorescence immediately increases by as much as 20,000-fold, rendering the FAP fusion proteins highly fluorescent. Moreover, since fluorogens can be made membrane impermeant, fluorescence can be limited to only those receptors expressed on the cell surface. Using cells expressing beta-2 adrenergic receptor (β2AR) fused at its N-terminus to a FAP, flow cytometry based receptor internalization assays have been developed and characterized. The fluorogen/FAP system is ideally suited to the study of cell surface proteins by fluorescence and avoids drawbacks of using receptor/fluorescent protein fusions, such as internal accumulation. We also briefly comment on extending FAP-based technologies to the study of events occurring inside of the cell as well.

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Acute hypoxia increases heart rate (HR) and cardiac output (Qt) at a given oxygen consumption (VO2) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac beta receptors. Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and Qt during hypoxic exercise. To test this, we separately blocked the beta-sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean +/- S.E.M. age = 31.7+/-1.6 years, normoxic maximal VO2 (VO2,max)=3.1+/-0.3 l min(-1)) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction=0.125) to VO2,max. Data were collected on different days under the following conditions: (1)control, (2) after 8.0 mg propranolol i.v. and (3) after 0.8 mg glycopyrrolate i.v. Qt was measured using open-circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a given VO2 (P<0.05, P<0.01 and P=0.2, respectively). HR/VO2 and Qt/VO2 increased during hypoxia in all three conditions (P<0.05). Unexpectedly, the effects of hypoxia on HR and Qt were not significantly different from control with either beta-sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and Qt do not necessarily require intact cardiac muscarinic and beta receptors. It may be that cardiac alpha receptors play a primary role in elevating HR and Qt during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked.

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Our study highlights the possibility of starting propranolol in an ambulatory way, establishes a dose of 2mg/kg/day and confirms the security profile of the drug. We consider propranolol as a first line treatment for IH.

inderal overdose treatment

Recent research has indicated serotonergic and dopaminergic abnormalities in the superior temporal gyrus of patients with a history of chronic auditory hallucinations. Both loxapine and aripiprazole have effects on dopaminergic and postsynaptic serotonergic (5-HT₂A) receptor systems, which could account for synergistic effects in treating refractory hallucinations. The combination appears safe, even when loxapine is given in high dosages. Patients should be monitored for the development of parkinsonian tremors.

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Because of their spontaneous involution, most infantile haemangiomas (IH) do not require therapeutic intervention. However, in 10 to 15% of cases such as segmental and multifocal IH, locations in the periocular, airway and perineal areas, or complications of ulceration, treatment is necessary. Moreover, the risk of permanent scarring and disfigurement associated with IH, even if involution is complete, has been increasingly recognized as a rationale for treatment. Treatments for IH currently include topical, intralesional, systemic therapies, laser and surgical modalities depending on the clinical scenario. However, clinicians must carefully weigh the risks and benefits for each treatment. Recently, the efficacy of propranolol, a non-cardioselective beta-blocker, was reported and has been revolutionary in the management of IH.

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Thirty-six patients with cirrhosis and ascites (decompensated group), 39 patients with cirrhosis but no ascites (compensated group) and 25 patients with normal renal and hepatic functions (control group) were studied. All had normal blood urea nitrogen and serum creatinine levels. The renal resistive index was calculated in all patients before and after oral propranolol treatment.

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Six aerobically trained male athletes and six healthy male individuals with similar ages and normal rest electrocardiograms were studied. Maximal oxygen uptake (O(2)max) was measured by cardiopulmonary testing. The sinus cycle length (SCL), AV conduction intervals, sinus node recovery time (SNRT), Wenckebach cycle (WC) and anterograde effective refractory period (ERP) of the AV node were evaluated by invasive electrophysiologic studies at baseline, after intravenous atropine (0.04 mg/kg) and after addition of intravenous propranolol (0.2 mg/kg).

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Hpts had rapidly developing secondary resistance and pseudotolerance to propranolol antianginal effect, bad tolerability of the drug.

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The effects of a commercially available saw palmetto extract were examined on the contractility of rat-isolated prostate glands. The extract was tested in the presence and absence of phentolamine, prazosin, yohimbine, propranolol, hexamethonium, cocaine, desipramine, nifedipine, guanethidine, atropine, and alpha,beta-methylene ATP to evaluate the mechanism of action. Isolated preparations of rat vas deferens and bladder were used for comparison.

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inderal with alcohol 2017-02-28

Oral health complications in diabetes Voltaren Medicine Information and hypertension include decreased salivary secretion. The sodium-glucose cotransporter 1 (SGLT1) protein, which transports 1 glucose/2 Na+/264 H2O molecules, is described in salivary glands. We hypothesized that changes in SGLT1 expression in the luminal membrane of ductal cell may be related to an altered salivary flow.

inderal high dose 2015-08-24

The actions of different adrenoceptor antagonists on gastric potential difference (PD), electrical current (I) and resistance (R) were studied, using the voltage clamp technique. In an isolated gastric mucosal tissue, 5% ethanol was able to reduce the PD and I across the gastric mucosa. Direct incubation with propranolol 10(-4) mol/l either from the mucosal or submucosal sides attenuated such effects. Intraperitoneal administration of propranolol (2.5-10 mg/kg), a nonselective beta-adrenoceptor blocker with significant membrane-stabilizing activity, given 30 min before Inderal Dosage the preparation of the gastric tissue, not only alleviated the fall in PD and I across the gastric mucosa, but also increased the R of the stomach tissue. Butoxamine, a selective beta2-antagonist, produced the similar but less significant effects in the same experimental setting. Metroprolol, a beta1-adrenoceptor blocker, given by the similar doses did not produce significant effects. Nonselective beta-adrenoceptor blocker, nadolol but not the beta- and alpha-adrenoceptor blocker, labetalol, also significantly preserved the decrease of PD induced by ethanol, but to a lesser extent. These findings suggest that blockade of the beta2-receptors in the gastric mucosa together with membrane-stabilizing activity could improve the integrity of the gastric mucosa, and these effects are probably acting through its direct action on the tissue.

inderal pills 2017-12-18

In NMR diffusion experiments to study ligand-protein binding equilibria, the spectral background due to broad protein resonances can contribute significantly to the measured ligand signal intensity resulting in erroneous binding affinities. One method to suppress the protein spectral background involves coupling a CPMG pulse train before or after the BPPSTE pulse sequence to allow for differential T(2) relaxation of the broad protein resonances. Here, we present an improved method, the Gradient Phase Encoded Spin-lock (GraPES) experiment that integrates the relaxation filter into the diffusion period. Compared with sequential CPMG-BPPSTE pulse sequences, GraPES offers effective suppression Requip Drug Classification of the protein background with improved signal-to-noise ratios and shorter experiment times.

inderal brand name 2016-09-12

Three of the four children showed a dramatic response to treatment with propranolol. However, one child responded initially but Trileptal Max Dose was readmitted with stridor secondary to new haemangioma proliferation.

inderal 80 mg 2017-04-15

Only 22% of small screenings-diagnosed AAA were treatable with propranolol for two years. Consequently, only large scale studies are capable of showing potential minor inhibition of expansion by Zofran 300 Mg propranolol. However, whether such treatment ever becomes ethically acceptable is debatable.

inderal dosage anxiety 2017-10-12

Beta-adrenoceptor antagonists are widely used in cardiovascular medicine. However, the main side effect of these drugs is due to antagonism of beta(2)-adrenoceptors in the airways, resulting in bronchospasm. Therefore, more cardioselective beta-blockers have been developed to offer a lower side effect profile. We have studied a new aryloxypropanolamine derivative (PP-34) with more cardioselectivity and efficacy against ischaemia/reperfusion injury in rats. Oxalate salts of 1-(tert-butylamino)-3-(5-tert-butylaminomethyl-2-methoxyphenoxy) propan-2-ol (PP-34) is a novel beta-adrenoceptor antagonist. In-vitro studies in rat isolated right atria, guinea-pig trachea and rat distal colon preparations were carried out to investigate the potency of PP-34 towards different beta-adrenoceptor subtypes. pA(2)/pK(B) values of PP-34 for beta(1), beta(2), and beta(3) adrenoceptor were 7.89+/-0.15, 6.13+/-0.09 and Artane 20 Mg 6.30+/-0.19, respectively. The beta(1)/beta(2) selectivity ratio calculated was in the order of PP-34 > atenolol > propranolol. Pre-ischaemic administration (20 min before coronary occlusion) of PP-34 (0.3 or 1 mg kg(-1)) showed cardioprotective effects against ischaemia/reperfusion injury in rats and significantly reduced arrhythmias, infarct area and necrosis induced by ischaemia/reperfusion injury. The efficacy of PP-34 was found to be greater then atenolol. In conclusion, PP-34 is a cardioselective beta-adrenoceptor antagonist, possessing potent anti-arrhythmic and cardioprotective effects against ischaemia/reperfusion injury in rats.

inderal drug 2016-03-20

Our study found carvedilol to be more potent than propranolol and atenolol in inhibiting platelet aggregation and thromboxane B2 production. Benicar Generic Name This may be due to the different structure and more convenient physico-chemical parameters of the carvedilol molecule.

inderal tablets 10mg 2015-09-30

Fibroblasts from the gingiva and the periodontal Periactin 4mg Dose ligament were exposed to agonists of the β-adrenergic receptors; isoproterenol (ISO, non-selective β-adrenergic agonist), salbutamol (SAL, selective β2-adrenergic receptor agonist) and BRL 37344 (BRL selective β3-receptor agonist). Proliferation was stimulated with platelet-derived growth factor-BB (PDGF-BB). Pharmacological inhibitors and gene expression analysis further revealed β-adrenergic signalling.

inderal 40 tablet 2015-01-26

In this paper we have studied the influence of a well-established rat model of periodontitis on resting and adrenergic-stimulated mucin secretion from rat submandibular glands. The selective beta(1)-receptor subtype agonist, dobutamine, induced mucin secretion while the selective Deltasone Buy beta(2)-, alpha(1)- and alpha(2)-agonists, soterenol, phenylephrine and clonidine, respectively, did not. In rats subjected to ligature-induced periodontitis mucin release, under unstimulated conditions (basal values), was significantly increased. This increment was abolished in the presence of propranolol and atenolol. Isoproterenol, concentration-dependent, increased mucin release in control and in ligature-induced periodontitis rats. Maximal effect of isoproterenol was decreased in rats with ligature while EC(50) was increased. Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. The inhibition of adenylyl cyclase by SQ 22536 resulted in a right shift of isoproterenol concentration-response curves in both groups, control and with ligature and returned basal values of rats with ligature to control ones. beta-Receptor population was decreased in submandibular gland membranes from rats with ligature without changes in affinity. Potencies of the beta-receptor antagonists in the competition studies were similar in both groups under study, control and with ligature. We conclude that in rats subjected to ligature-induced periodontitis unstimulated mucin secretion is increased. The increment seems to be due to an activation of the sympathetic system since it is inhibited by the beta-adrenoceptors antagonists and by the inhibition of the adenylyl cyclase. We can speculate that inflammatory mediators from the experimental periodontitis could be involved in the mechanism underlying the activation of the sympathetic system.