Beta-1 adrenergic receptors

The in vitro effect of nifedipine and atenolol, either alone or in combination, on the proliferation and migration of rat aortic smooth muscle cells was investigated. Nifedipine inhibited the replication of arterial myocytes in concentrations ranging between 10 and 100 microM. The inhibition, evaluated as cell number, was dose- and time-dependent with an IC50 of 39 and 34 microM after 48 and 72 h, respectively; the cell doubling time increased with drug concentrations up to 118 h versus 28 h for controls. Atenolol alone failed to reduce arterial myocyte proliferation, and did not influence the effect of nifedipine on cell proliferation. Nifedipine and atenolol alone inhibited in a dose-dependent manner rat aortic myocytes migration induced by fibrinogen as chemotactic agent. When the combination nifedipine-atenolol was investigated, an additive inhibitory effect on cell migration was observed. These results provide in vitro support for a potential effect of this drug association on early steps of atherogenesis.[3]

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Hem-ECs treated with either propranolol, atenolol or metoprolol displayed positive LysoTracker Red staining. Increased LC3BII/LC3BI ratio, as well as p62 modulation, were documented in β-blockers treated Hem-ECs. Abundant autophagic vacuoles and multilamellar bodies characterized the cytoplasmic ultrastructural features of autophagy in cultured Hem-ECs exposed in vitro to β-blocking agents. Importantly, similar biochemical and morphologic evidence of autophagy were observed following rapamycin while Bafilomycin A1 significantly prevented the autophagic flux promoted by β-blockers in Hem-ECs. Conclusion: Our data suggest that autophagy may be ascribed among the mechanisms of action of β-blockers suggesting new mechanistic insights on the potential therapeutic application of this class of drugs in pathologic conditions involving uncontrolled angiogenesis [4].

Compared with BP before medication, all 3 doses of combined atenolol and amlodipine significantly decreased the BP at 24 h after administration, except for the low dose on diastolic BP. Compared with the control group, all 3 doses of combined atenolol and amlodipine significantly reduced the average BP levels for the 24 h period after administration; furthermore, the high and intermediate doses also significantly decreased the BPV levels for the same period. The q values calculated by probability sum analysis for systolic and diastolic BP for the 24 h period after administration were 2.29 and 1.45, respectively, and for systolic and diastolic BPV for the same period they were 1.41 and 1.60, respectively. Conclusion: There is significant synergism between atenolol and amlodipine in lowering and stabilizing BP in 2K1C renovascular hypertensive rats [5].

Fresh tissue specimens, surgically removed for therapeutic purpose to seven children affected by proliferative IH, were subjected to enzymatic digestion. Cells were sorted with anti-human CD31 immunolabeled magnetic microbeads. Following phenotypic characterization, expanded Hem-ECs, at P2 to P6, were exposed to different concentrations (50 μM to 150 μM) of propranolol, atenolol or metoprolol alone and in combination with the autophagy inhibitor Bafilomycin A1. Rapamycin, a potent inducer of autophagy, was also used as control. Autophagy was assessed by Lysotracker Red staining, western blot analysis of LC3BII/LC3BI and p62, and morphologically by transmission electron microscopy [4].

Aim: To test the synergistic effects of atenolol and amlodipine on lowering blood pressure (BP) and reducing blood pressure variability (BPV) in 2-kidney, one-clip (2K1C) renovascular hypertensive rats. Methods: Forty-eight 2K1C renovascular hypertensive rats were randomly divided into 6 groups. They were respectively given 0.8% carboxymethylcellulose sodium (control), atenolol (10.0 mg/kg), amlodipine (1.0 mg/kg), and combined atenolol and amlodipine (low dose: 5.0+0.5 mg/kg; intermediate dose: 10.0+1.0 mg/kg; high dose: 20.0+2.0 mg/kg). The drugs were given via a catheter in a gastric fistula. BP was recorded for 25 h from 1 h before drug administration to 24 h after administration.[5]

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Animals and RVHR preparation [5]
Male Sprague–Dawley rats (160–180 g) were anesthetized with a combination of ketamine (40 mg/kg) and diazepam (6 mg/kg). The right renal artery of each animal was isolated through a flank incision as described previously, and a silver clip (0.2 mm internal gap) was placed on the renal artery. Five weeks after placement of the clip, the systolic blood pressure (SBP) of rats was measured by using the tail-cuff method (CB10). In total, 48 RVHR whose SBP was greater than 160 mmHg were used in this study. Rats were kept in a controlled temperature (23 °C– 25 °C) and lighting (light 08:00–20:00, dark 20:00–08:00) environment, and had free access to food and tap water. All the animals used in this work received humane care in compliance with institutional animal care guidelines.

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BP and BPV measurement [5]
SBP, diastolic blood pressure (DBP) and heart period (HP) were continuously recorded using a previously described technique. Briefly, rats were anesthetized by injection (ip) with a combination of ketamine (40 mg/kg) and diazepam (6 mg/kg). A floating polyethylene catheter was inserted into the lower abdominal aorta via the left femoral artery for BP measurement, and another catheter was placed into the stomach via a mid-abdominal incision for drug administration. The catheters were exteriorized through the interscapular skin. After a 2-d recovery period, the animals were placed for BP recording in individual cylindrical cages containing food and water. The aortic catheter was connected to a BP transducer via a rotating swivel that allowed the animals to move freely in the cage. After approximately 14-h habituation, at 9:00 o’clock the BP signal was begun to be digitized by a microcomputer. One hour later, at 10:00 o’clock the drug was given via the catheter in the gastric fistula. SBP, DBP, and HP values were recorded beat-to-beat for 25 h, up to 10:00 o’clock on the second day. The mean values of these parameters during a designated period were calculated and served as SBP, DBP and HP values. The standard deviation of all values obtained over 24 h was denoted as the quantitative parameter of variability; that is, SBP variability (SBPV), DBP variability (DBPV), and HP variability (HPV) for each rat.

Absorption, Distribution and Excretion
Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, with the remainder being excreted unchanged in the feces. Administering atenolol with food can decrease the AUC by about 20%. While atenolol can cross the blood-brain barrier, it does so slowly and to a small extent.
85% is eliminated by the kidneys following IV administration with 10% appearing in the feces.
Total Vd of 63.8-112.5 L. Atenolol distributes into a central volume of 12.8-17.5 L along with two peripheral compartments with a combined volume of 51-95 L. Distribution takes about 3 hrs for the central compartment, 4 hrs for the shallower peripheral compartment, and 5-6 hrs for the deeper peripheral compartment.
Total clearance is estimated at 97.3-176.3 mL/min with a renal clearance of 95-168 mL/min.
In animals, atenolol is well distributed into most tissues and fluids except brain and /cerebrospinal fluid/. Unlike propranolol, only a small portion of atenolol is apparently distributed into the CNS.
Approximately 5-15% of atenolol is bound to plasma protein.
Atenolol readily crosses the placenta, and has been detected in cord blood. During continuous administration, fetal serum concentrations of the drug are probably equivalent to those in maternal serum. Atenolol is distributed into milk; peak milk concentrations of the drug are higher than peak serum concentrations after an individual dose, and the area under the milk concentration-time (AUC) is substantially greater than that of the serum AUC in lactating women receiving the drug continuously.
Atenolol is rapidly but incompletely absorbed from the GI tract. Only about 50-60% of an oral dose of atenolol is absorbed. In healthy adults, peak plasma concentrations of 1-2 ug/ml are achieved 2-4 hours after oral administration of a single 200 mg dose of atenolol. An approximately fourfold interindividual variation in plasma concentrations attained has been reported with a specific oral dose of atenolol. Peak plasma atenolol concentrations are achieved within 5 minutes following direct IV injection of the drug, and decline rapidly during an initial distribution phase; after the first 7 hours, plasma concentrations reportedly decline with an elimination half-life similar to that of orally administered drug.
For more Absorption, Distribution and Excretion (Complete) data for ATENOLOL (6 total), please visit the HSDB record page.

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Metabolism / Metabolites
Minimal metabolism in the liver. The sole non-conjugated metabolite is the product of a hydroxylation reaction at the carbon between the amide and benzene groups. The only other metabolite to be confirmed is a glucuronide conjugate. These metabolites make up 5-8% and 2% of the renally excreted dose with 87-90% appearing as unchanged drug. The hydroxylated metabolite is exerts 1/10th the beta-blocking activity of atenolol.
Minimal hepatic metabolism; removable by hemodialysis; very low lipid solubility.
Little or no metabolism of atenolol occurs in the liver. Approximately 40-50% of an oral dose of the drug is excreted in urine unchanged. The remainder is excreted unchanged in feces, principally as unabsorbed drug. About 1-12% of atenolol is reportedly removed by hemodialysis.
Hepatic (minimal)
Route of Elimination: Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Unlike propranolol or metoprolol, but like nadolol, atenolol undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion.
Half Life: 6-7 hours

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Biological Half-Life
6-7 hrs.
In patients with normal renal function, atenolol has a plasma half-life (t1/2) of 6-7 hours. Children with normal renal function may exhibit a shorter elimination half-life. In one study in children ages 5-16 (mean: 8.9) with arhythmias and normal renal and hepatic function, the terminal elimination half-life averaged 4.6 hours. Plasma t1/2 of the drug increases to 16-27 hours in patients with creatinine clearances of 15-35 ml/minute per 1.73 sq m and exceeds 27 hours with progressive renal impairment.
The half-life in the elderly was significantly longer (8.8 + or - 0.9 hr) compared with that in the young (5.8 + or - 1.1 hr) (p < 0.01).

Hepatotoxicity
Atenolol therapy has been associated with mild-to-moderate elevations of serum aminotransferase levels in 1% to 2% of patients. These elevations, however, are usually asymptomatic and transient and resolve even with continuation of therapy. A few instances of clinically apparent, acute liver injury attributable to atenolol have been reported. In view of its wide scale use, atenolol induced liver injury is exceedingly rare. The onset of injury has been within 1 to 4 weeks and pattern of liver enzyme elevations has been hepatocellular or mixed. Symptoms of hypersensitivity (rash, fever, eosinophilia) are uncommon as is autoantibody formation. Most cases are self-limiting and resolve rapidly once atenolol is stopped; however, at least one fatal instance has been reported.
Likelihood score: D (Possible rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because of atenolol's relatively extensive excretion into breastmilk and its extensive renal excretion, other agents may be preferred while nursing a newborn or preterm infant or with high maternal dosages. Infants older than 3 months of age appear to be at little risk of adverse effects from atenolol in breastmilk. Timing breastfeeding with respect to the time of the atenolol dose appears to be of little benefit in reducing infant atenolol exposure because the time of the peak is unpredictable.
◉ Effects in Breastfed Infants
A study of mothers taking beta-blockers during nursing found a numerically, but not statistically significant increased number of adverse reactions in those taking any beta-blocker. Although the ages of infants were matched to control infants, the ages of the affected infants were not stated. Of 13 mothers taking atenolol, one reported lethargy in her breastfed infant; she was also taking other unspecified drugs for hypertension.
Cyanosis, bradycardia and hypothermia occurred in a 5-day-old infant probably because of atenolol in breastmilk. Her mother was taking atenolol 50 mg twice daily. Symptoms continued until day 8 when breastfeeding was discontinued.
No difference between resting and crying heart rates were observed in 22 breastfed (extent not stated) infants aged 3 to 4 months whose mothers were taking atenolol in an average oral dosage of 49 mg daily. This finding indicated that the infants were experiencing no beta-adrenergic blockade from atenolol in breastmilk.
Other authors have reported 15 infants aged 3 days to 2 weeks exposed to atenolol in breastmilk with no signs of adverse effects. Maternal dosages were 50 or 100 mg daily.
◉ Effects on Lactation and Breastmilk
One unusual case of oligomenorrhea, hyperprolactinemia and galactorrhea was reported in a 38-year-old woman who had been taking atenolol for about 18 months. Prolactin values returned to normal within 3 days of discontinuation of atenolol. Galactorrhea slowly lessened and disappeared one month after atenolol discontinuation.
◈ What is atenolol?
Atenolol is a medication that has been used to treat high blood pressure, chest pain (angina), and heart rhythm issues (arrythmias). It has also been used to treat, prevent, and improve survival after a heart attack. It belongs to the class of medications called beta-blockers. A brand name for atenolol is Tenormin®.Sometimes when people find out they are pregnant, they think about changing how they take their medication, or stopping their medication altogether. However, it is important to with your healthcare providers before making any changes to how you take this medication. Your healthcare providers can talk with you about the benefits of treating your condition and the risks of untreated illness during pregnancy.
◈ I take atenolol. Can it make it harder for me to get pregnant?
It is not known if atenolol can make it harder to get pregnant.
◈ Does taking atenolol increase the chance for miscarriage?
Miscarriage is common and can occur in any pregnancy for many different reasons. Studies have not been done to see if atenolol increases the chance for miscarriage.
◈ Does taking atenolol increase the chance of birth defects?
Every pregnancy starts out with a 3-5% chance of having a birth defect. This is called the background risk. Studies have not been done to see if atenolol increases the chance for birth defects.
◈ Does taking atenolol in pregnancy increase the chance of other pregnancy-related problems?
Atenolol has been linked with reduced growth of the fetus (smaller in size and/or low birth weight). It is not clear if this happens because of the medication, the condition being treated, or other factors. One study did find that atenolol can directly affect blood flow through the placenta, which might be linked with poor growth of the fetus, causing low birth weight (weighing less than 5 pounds, 8 ounces [2500 grams] at birth).
◈ Does taking atenolol in pregnancy affect future behavior or learning for the child?
Studies have not been done to see if atenolol can cause behavior or learning issues for the child.
◈ Breastfeeding while taking atenolol:
Atenolol passes into breastmilk. There have been reports of babies with slow heart rate, low blood pressure, a bluish color in the skin due to a lack of oxygen in the blood (cyanosis), and low body temperature after being exposed to atenolol through breast milk. If you suspect the baby has any symptoms (slow heart rate, low blood pressure, a bluish color in the skin, lips, or fingernails) contact the child’s healthcare provider.The product label for atenolol recommends people who are breastfeeding not use this medication. But, the benefit of using atenolol may outweigh possible risks. Your healthcare providers can talk with you about using atenolol and what treatment is best for you. Be sure to talk to your healthcare provider about all of your breastfeeding questions.
◈ If a male takes atenolol, could it affect fertility (ability to get partner pregnant) or increase the chance of birth defects?
Based on the studies reviewed, it is not known if atenolol could affect male fertility or increase the chance of birth defects above the background risk. In general, exposures that fathers or sperm donors have are unlikely to increase risks to a pregnancy. For more information, please see the MotherToBaby fact sheet on Paternal Exposures at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

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Protein Binding
6-16% bound in plasma. Atenolol binds to two sites on human serum albumin.

[1]. Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension. Drugs. 1979;17(6):425-460.

[2]. (+/-)[125Iodo] cyanopindolol, a new ligand for beta-adrenoceptors: identification and quantitation of subclasses of beta-adrenoceptors in guinea pig. Naunyn Schmiedebergs Arch Pharmacol. 1981;317(4):277-285.

[3].Effect of the nifedipine-atenolol association on arterial myocyte migration and proliferation. Pharmacol Res. 1993 May-Jun;27(4):299-307.

[4].Β-blockers activate autophagy on infantile hemangioma-derived endothelial cells in vitro. Vascul Pharmacol. 2022 Oct;146:107110.

[5].Synergistic effects of atenolol and amlodipine for lowering and stabilizing blood pressure in 2K1C renovascular hypertensive rats. Acta Pharmacol Sin. 2005 Nov;26(11):1303-8.

Atenolol is a beta-selective (cardioselective) adrenoceptor blocking drug without partial agonist or membrane stabilising activity. Its profile of action most closely resembles that of metoprolol which differs only in that it has some membrane stabilising activity. Atenolol has been well studied and is effective in the treatment of hypertension and in the prophylactic management of angina. Its narrow dose response range obviates the need for highly individualised dose titration. In patients with angina its long duration of beta-blocking activity allows once daily dosage, whereas other beta-blockers, unless in sustained release dosage forms, need to be given in divided doses. Other beta-blockers can be given once daily in hypertension, but at presnt the evidence for effective control with a once daily regimen is more convincing with atenolol. Further studies are need to clarify any important differences in blood pressure control between the various beta-blocking drugs, both in conventional or sustained release dosage forms. As with metoprolol, atenolol is preferable to non-selective beta-blockers in patients with asthma or diabetes mellitus. Atenolol has been well tolerated in most patients, its profile of adverse reactions generally resembling that of other beta-blocking drugs, although its low lipid solubility and limited penetration into the brain results in a lower incidence of central nervous system effects than seen with propranolol. Atenolol is eliminated virtually entirely as unchanged drug in the urine and dosage needs to be reduced in patients with moderate to severely impaired renal function (glomerular filtration rate less than 30 ml/min). There is no need for modification of dosage of atenolol in liver disease.[1]

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Atenolol can cause developmental toxicity according to state or federal government labeling requirements.
Atenolol is an ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent. It has a role as a beta-adrenergic antagonist, an anti-arrhythmia drug, an antihypertensive agent, a sympatholytic agent, a xenobiotic and an environmental contaminant. It is a member of ethanolamines, a monocarboxylic acid amide and a propanolamine.
Atenolol is a cardioselective beta-blocker used in a variety of cardiovascular conditions. Sir James Black, a Scottish pharmacologist, pioneered the use of beta-blockers for the management of angina pectoris in 1958 for which he received the Nobel Prize. Beta-blockers quickly became popular in clinical use and where subsequently investigated for use in myocardial infarction, arrhythmias, and hypertension during the 1960s. Later they continued to be investigated for use in heart failure throughout the 1970-1980s. Atenolol itself was developed early on in this history by Alvogen Malta under the trade name Tenormin and received FDA approval in September, 1981. Despite being one of the most widely prescribed beta blockers, evidence suggests atenolol may not significantly reduce mortality, and only modestly reduce the risk of cardiovascular disease in patients with hypertension. A Cochrane review of patients being treated for primary hypertension shows that atenolol shows a risk ratio of 0.88 for cardiovascular disease risk and a risk ratio of 0.99 for mortality. Similar results have been found in other meta-analyses. A meta-analysis of over 145,000 patients showed the risk of stroke in patients taking atenolol may depend on the age of the patient. The use of atenolol may need to be based on more patient factors than hypertension alone.
Atenolol is a beta-Adrenergic Blocker. The mechanism of action of atenolol is as an Adrenergic beta-Antagonist.
Atenolol is a cardioselective beta-blocker that is widely used in the treatment of hypertension and angina pectoris. Atenolol has been linked to rare cases of drug induced liver injury, some of which have been fatal.
Atenolol is a synthetic isopropylamino-propanol derivative used as an antihypertensive, hypotensive and antiarrhythmic Atenolol acts as a peripheral, cardioselective beta blocker specific for beta-1 adrenergic receptors, without intrinsic sympathomimetic effects. It reduces exercise heart rates and delays atrioventricular conduction, with overall oxygen requirements decreasing. (NCI04)
Atenolol is a so-called beta1-selective (or 'cardioselective') drug. That means that it exerts greater blocking activity on myocardial beta1-receptors than on beta2 ones in the lung. The beta2 receptors are responsible to keep the bronchial system open. If these receptors are blocked, bronchospasm with serious lack of oxygen in the body can result. However, due to its cardioselective properties, the risk of bronchospastic reactions if using atenolol is reduced compared to nonselective drugs as propranolol. Nonetheless, this reaction may also be encountered with atenolol, particularly with high doses. Extreme caution should be exerted if atenolol is given to asthma patients, who are particularly at risk; the dose should be as low as possible. If an asthma attack occurs, the inhalation of a beta2-mimetic antiasthmatic, such as hexoprenalin or salbutamol, will usually suppress the symptoms. Atenolol (trade name Tenormin) can be used to treat cardiovascular diseases such as hypertension, coronary heart disease, arrhythmias, and treatment of myocardial infarction after the acute event. Patients with compensated congestive heart failure may be treated with atenolol as a co medication (usually together with an ACE inhibitor, a diuretic and a digitalis-glycoside, if indicated). In patients with congestive heart failure, it reduces the need for and the consumption of oxygen of the heart muscle. It is very important to start with low doses, as atenolol reduces also the muscular power of the heart, which is an undesired effect in congestive heart failure.
A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.
See also: Atenolol; Chlorthalidone (component of); Atenolol; scopolamine hydrobromide (component of).

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Drug Indication
**Indicated** for: 1) Management of hypertension alone and in combination with other antihypertensives. 2) Management of angina pectoris associated with coronary atherosclerosis. 3) Management of acute myocardial infarction in hemodynamically stable patients with a heart rate greater than 50 beats per minutes and a systolic blood pressure above 100 mmHg. **Off-label** uses include: 1) Secondary prevention of myocardial infarction. 2) Management of heart failure. 3) Management of atrial fibrillation. 4) Management of supraventricular tachycardia. 5) Management of ventricular arrythmias such as congenital long-QT and arrhythmogenic right ventricular cardiomyopathy. 6) Management of symptomatic thyrotoxicosis in combination with [methimazole]. 7) Prophylaxis of migraine headaches. 8) Management of alcohol withdrawal.
FDA Label

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Mechanism of Action
Atenolol is a cardioselective beta-blocker, called such because it selectively binds to the β1-adrenergic receptor as an antagonist up to a reported 26 fold more than β2 receptors. Selective activity at the β1 receptor produces cardioselectivity due to the higher population of this receptor in cardiac tissue. Some binding to β2 and possibly β3 receptors can still occur at therapeutic dosages but the effects mediated by antagonizing these are significantly reduced from those of non-selective agents. β1 and β2 receptors are G_s coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA). In cardiomyocytes PKA is thought to mediate activation of L-type calcium channels and ryanodine receptors through their phosphorylation. L-type calcium channels can then provide an initial rise in intracellular calcium and trigger the ryanodine receptors to release calcium stored in the sarcoplasmic reticulum (SR) and increased contractility. PKA also plays a role in the cessation of contraction by phosphorylating phospholamban which in turn increases the affinity of SR Ca²⁺ ATPase to increase reuptake of calcium into the SR. It also phophorylates troponin I to reduce affinity of the protein for calcium. Both of these events lead to a reduction in contraction which, when coupled with the initial increase in contraction, allows for faster cycling and consequently higher heart rate with increased contractility. L-type calcium channels are also a major contributor to cardiac depolarization and their activation can increase frequency of action potentials and possibly the incidence of ectopic potentials. Similar inihibitory events occur in the bronchial smooth muscle to mediate relaxation including phosphorylation of myosin light-chain kinase, reducing its affinity for calcium. PKA also inhibits the excitatory G_q coupled pathway by phosphorylating the inositol trisphosphate receptor and phospholipase C resulting in inhibition of intracellular calcium release. Antagonism of this activity by beta-blocker agents like atenolol can thus cause increased bronchoconstriction.
By inhibiting myocardial beta 1-adrenergic receptors, atenolol produces negative chronotropic and inotropic activity. The negative chronotropic action of atenolol on the sinoatrial node results in a decrease in the rate of sinoatrial node discharge and an increase in recovery time, thereby decreasing resting and exercise stimulated heart rate and reflex orthostatic tachycardia by about 25-35%. High doses of the drug may produce sinus arrest, especially in patients with sinoatrial node disease (eg, sick sinus syndrome). Atenolol also slows conduction in the atrioventricular nose. Although stroke index may be increased moderately by about 10%, atenolol usually reduces cardiac output by about 20% probably secondary to its effect on heart rate. The decrease in myocardial contractability and heart rate, as well as the reduction in blood pressure, produced by atenolol generally lead to a reduction in myocardial oxygen consumption which accounts for the effectiveness of the drug in chronic stable angina pectoris; however, atenolol can increase oxygen requirements by increasing left ventricular fiber length and end-diastolic pressure, particularly in patients with cardiac failure.
Atenolol suppresses plasma renin activity and suppresses the renin aldosterone angiotensin system.
The toxic actions of beta-blockers appear to be related to properties such as membrane depressant activity and possibly due to actions on beta-adrenoceptors distinct from those in the cardiovascular system.

302.79702

302.14

C, 55.53; H, 7.66; Cl, 11.71; N, 9.25; O, 15.85

51706-40-2

Atenolol-d7;1202864-50-3; 51706-40-2 (HCl); 29122-68-7;93379-54-5 (S isomer); 56715-13-0 (R isomer)

119274

Typically exists as solid at room temperature

1.125g/cm3

508ºC at 760mmHg

261.1ºC

2.794

4

4

8

20

263

0

CC(C)NCC(COC1=CC=C(C=C1)CC(=O)N)O.Cl

FFDDLJYKJQGSPW-UHFFFAOYSA-N

InChI=1S/C14H22N2O3.ClH/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18;/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18);1H

2-[4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl]acetamide;hydrochloride

Atenolol hydrochloride; 51706-40-2; Atenolol HCl; dl-Atenolol.HCl; 4-[2-HYDROXY-3-[(ISOPROPYL)AMINO]PROPOXY]PHENYLACETAMIDE HYDROCHLORIDE; 6DI0UT7U1Q; 4-(2-Hydroxy-3-((isopropyl)amino)propoxy)phenylacetamide hydrochloride; 2-[4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl]acetamide hydrochloride;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)