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 the oral dose is absorbed through the gastrointestinal tract, with the remainder excreted unchanged in the feces. Co-administration with food can reduce the AUC of atenolol by approximately 20%. While atenolol can cross the blood-brain barrier, the process is slow and minimal. Following intravenous administration, 85% of the drug is excreted by the kidneys, and 10% by the feces. The total volume of distribution is 63.8–112.5 L. Atenolol is distributed in the central compartment (12.8–17.5 L) and two peripheral compartments (total volume 51–95 L). Distribution to the central compartment takes approximately 3 hours, to the shallower peripheral compartments approximately 4 hours, and to the deeper peripheral compartments approximately 5–6 hours. The estimated total clearance is 97.3–176.3 mL/min, and the renal clearance is 95–168 mL/min. In animal studies, atenolol distributes well in most tissues and fluids, except for brain tissue and cerebrospinal fluid. Unlike propranolol, atenolol is distributed only in small amounts in the central nervous system. Approximately 5-15% of atenolol is bound to plasma proteins. Atenolol readily crosses the placenta and is detectable in umbilical cord blood. During continuous administration, fetal serum drug concentrations may be comparable to maternal serum drug concentrations. Atenolol is distributed in breast milk; after a single dose, peak drug concentrations in breast milk are higher than in serum, and in lactating women taking the drug continuously, the area under the concentration-time curve (AUC) in breast milk is significantly greater than that in serum. Atenolol is rapidly but incompletely absorbed from the gastrointestinal tract. After oral administration, only about 50-60% of atenolol is absorbed. In healthy adults, peak plasma drug concentrations can reach 1-2 μg/ml 2-4 hours after a single oral dose of 200 mg atenolol. It has been reported that after administration of atenolol at specific doses, inter-individual plasma concentrations vary by approximately fourfold. Following intravenous injection of atenolol, peak plasma concentrations are reached within 5 minutes and decline rapidly during the initial distribution phase; plasma concentrations are reported to decrease after 7 hours, with an elimination half-life similar to that of oral administration. For more complete data on the absorption, distribution, and excretion of atenolol (6 types), please visit the HSDB record page. Metabolites/Metabolites: Minimal metabolism in the liver. The only unconjugated metabolites are products of the carbon atom hydroxylation reaction between the amide group and the benzene ring. The only other confirmed metabolites are glucuronide conjugates. These metabolites account for 5-8% and 2% of the renal excretion dose, respectively, with the remaining 87-90% excreted unchanged. The β-receptor blocking activity of the hydroxylated metabolites is approximately one-tenth that of atenolol. Minimal hepatic metabolism; can be removed by hemodialysis; very low lipid solubility. Atenolol is almost not metabolized in the liver. Approximately 40-50% of orally administered doses of atenolol are excreted unchanged in the urine. The remainder is excreted unchanged in the feces, primarily as unabsorbed drug. It has been reported that approximately 1-12% of atenolol can be removed via hemodialysis.
Hepatic (very little)
Clearance route: Approximately 50% of orally administered doses are absorbed through the gastrointestinal tract, with the remainder excreted unchanged in the feces. Unlike propranolol or metoprolol, but similar to nadolol, atenolol is almost entirely not metabolized by the liver; the absorbed portion is primarily excreted through the kidneys.
Half-life: 6-7 hours
Biological half-life
6-7 hours.
In patients with normal renal function, the plasma half-life (t1/2) of atenolol is 6-7 hours. The elimination half-life may be shorter in children with normal renal function. A study of children aged 5–16 years (mean age: 8.9 years) with cardiac arrhythmias and normal renal and hepatic function showed a mean terminal elimination half-life of 4.6 hours. In patients with creatinine clearance of 15–35 ml/min/1.73 m², the plasma half-life (t1/2) increased to 16–27 hours, and exceeded 27 hours with progressive renal impairment. The half-life in older adults (8.8 ± 0.9 hours) was significantly longer than in younger adults (5.8 ± 1.1 hours) (p < 0.01).

Hepatotoxicity
Atenolol treatment is associated with mild to moderate elevations in serum transaminase levels in 1% to 2% of patients. However, these elevations are usually asymptomatic and transient, resolving with continued treatment. A few clinically significant atenolol-related acute liver injury cases have been reported. Given the widespread use of atenolol, liver injury caused by it is extremely rare. Injury usually develops within 1 to 4 weeks, with hepatocellular or mixed patterns of liver enzyme elevations. Hypersensitivity symptoms (rash, fever, eosinophilia) and autoantibody formation are uncommon. Most cases are self-limiting, resolving rapidly upon discontinuation of atenolol; however, at least one death has been reported. Probability Score: D (Possibly a rare cause of clinically significant liver injury).

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Effects during pregnancy and lactation
◉ Overview of medication use during lactation
Because atenolol is secreted in relAtevirdiney large quantities in breast milk and excreted by the kidneys in large quantities, other medications may be preferred when breastfeeding newborns or premature infants, or when the mother is taking high doses of atenolol. Infants older than 3 months appear unlikely to experience adverse reactions from atenolol in breast milk. Adjusting the timing of breastfeeding and atenolol administration appears to have little effect on reducing infant atenolol exposure, as the timing of peak drug levels is difficult to predict.
◉ Effects on breastfed infants
A study of breastfeeding mothers taking beta-blockers found a numerically increased number of adverse reactions in mothers taking any beta-blocker, but this was not statistically significant. Although the infants were age-matched to control groups, the age of affected infants was not specified. Among 13 mothers taking atenolol, one reported drowsiness in her breastfed infant; she was also taking other unspecified antihypertensive medications. A 5-day-old infant presented with cyanosis, bradycardia, and hypothermia, possibly due to atenolol in her breast milk. Her mother received 50 mg of atenolol twice daily. Symptoms persisted until day 8, at which point breastfeeding was discontinued. In 22 breastfed infants aged 3 to 4 months (breastfeeding extent not specified), no difference was observed in resting heart rate or crying heart rate; these infants' mothers received an average of 49 mg of atenolol orally daily. This finding suggests that infants do not experience β-adrenergic blockade from atenolol in breast milk. Other authors reported 15 infants aged 3 days to 2 weeks who were exposed to atenolol through breast milk without signs of adverse reactions. The mothers received either 50 or 100 mg daily.
◉ Effects on Lactation and Breast Milk
A rare case of oligomenorrhea, hyperprolactinemia, and galactorrhea was reported in a 38-year-old woman after taking atenolol for approximately 18 months. Prolactin levels returned to normal within 3 days of discontinuing atenolol. The galactorrhea symptoms gradually lessened and disappeared one month after discontinuing atenolol.
◈ What is Atenolol?
Atenolol is a medication used to treat high blood pressure, chest pain (angina), and arrhythmias. It is also used to treat and prevent heart attacks and to improve survival rates after a heart attack. It belongs to the beta-blocker class of drugs. The brand name for atenolol is Tenormin®. Sometimes, when people find out they are pregnant, they may consider changing their medication regimen or even stopping it entirely. However, it is essential to consult your healthcare provider before changing your medication regimen. Your healthcare provider can discuss with you the benefits of treating your condition and the risks of not treating the condition during pregnancy.
◈ I take atenolol. Will taking atenolol affect pregnancy?
It is currently unclear whether atenolol affects pregnancy.
◈ Will taking atenolol increase the risk of miscarriage?
Miscarriage is common and can occur in any pregnancy for a variety of reasons. There is currently no research indicating that atenolol increases the risk of miscarriage.
◈ Will taking atenolol increase the risk of birth defects?
There is a 3-5% risk of birth defects in each pregnancy, known as background risk. There is currently no research indicating that atenolol increases the risk of birth defects.
◈ Will taking atenolol during pregnancy increase the risk of other pregnancy-related problems?
Atenolol is associated with fetal growth restriction (smaller size and/or lower birth weight). It is currently unclear whether this is caused by the drug itself, the disease it treats, or other factors. One study found that atenolol can directly affect placental blood flow, which may be related to poor fetal growth and development, leading to low birth weight (birth weight less than 2500 grams).
◈ Will taking atenolol during pregnancy affect a child's future behavior or learning abilities?
Currently, there are no studies exploring whether atenolol causes behavioral or learning problems in children.
◈ Breastfeeding while taking atenolol:
Atenolol can pass into breast milk. There are reports that infants exposed to atenolol through breast milk may experience symptoms such as slowed heart rate, low blood pressure, cyanosis due to blood oxygen deficiency, and hypothermia. If you suspect your baby has any symptoms (slow heart rate, low blood pressure, blue skin, lips, or nails), please contact your child's healthcare provider. The product label for atenolol advises against using this medication while breastfeeding. However, the benefits of using atenolol may outweigh the potential risks. Your healthcare provider can discuss the use of atenolol with you and the best treatment option for you. Be sure to consult your healthcare provider about all your questions regarding breastfeeding.
◈ If men take atenolol, will it affect fertility (the ability to impregnate a partner) or increase the risk of birth defects? Based on reviewed studies, it is unclear whether atenolol affects male fertility or increases the risk of birth defects (above background risk). Generally, exposure to this drug by the father or sperm donor is unlikely to increase the risk of pregnancy. For more information, please see MotherToBaby's fact-sheets on paternal exposure at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/. Protein Binding: 6-16% of atenolol is bound to proteins 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 (cardiac-selective) adrenergic receptor blocker without partial agonist or membrane-stabilizing effects. Its mechanism of action is most similar to metoprolol, the only difference being that atenolol has some membrane-stabilizing effect. Atenolol is well-studied and effective in treating hypertension and preventing angina. It has a narrow dose-response range, eliminating the need for highly individualized dose titration. For angina patients, atenolol's long duration of beta-blocking allows for once-daily administration, while other beta-blockers (unless in extended-release formulations) require divided doses. Other beta-blockers can also be used once-daily to treat hypertension, but the evidence for the efficacy of once-daily dosing of atenolol is currently more robust. Further research is needed to clarify whether there are significant differences in blood pressure control among various beta-blockers (including conventional and extended-release formulations). Similar to metoprolol, atenolol is superior to non-selective beta-blockers for patients with asthma or diabetes. Most patients tolerate atenolol well, and its adverse reaction profile is similar to other β-blockers, but due to its low lipid solubility and limited brain penetration, the incidence of central nervous system adverse reactions is lower compared to propranolol. Atenolol is almost entirely excreted unchanged in the urine, and patients with moderate to severe renal impairment (glomerular filtration rate less than 30 ml/min) require dose reduction. No dose adjustment is required for patients with liver disease. [1]

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Atenolol may cause developmental toxicity depending on state or federal labeling requirements.
Atenolol is an ethanolamine compound with a (4-carbamoylmethylphenoxy)methyl group and an N-isopropyl substituent at the 1 position. It has multiple functions, including as a β-adrenergic antagonist, antiarrhythmic drug, antihypertensive drug, sympathomimetic drug, exogenous substance, and environmental pollutant. It belongs to the ethanolamine, monocarboxylic acid amide, and propanolamine classes. Atenolol is a cardioselective beta-blocker used to treat a variety of cardiovascular diseases. Sir James Black, a Scottish pharmacologist, was awarded the Nobel Prize in 1958 for pioneering the use of beta-blockers in treating angina. Beta-blockers were rapidly adopted in clinical practice and were investigated in the 1960s for treating myocardial infarction, arrhythmias, and hypertension. Later, in the 1970s and 1980s, their application in treating heart failure was further investigated. Atenolol was initially developed by Alvogen Malta under the brand name Tenormin and was approved by the U.S. Food and Drug Administration (FDA) in September 1981. Although it is one of the most prescribed beta-blockers, there is evidence that atenolol may not significantly reduce mortality and may only slightly reduce the risk of cardiovascular disease in patients with hypertension. A Cochrane systematic review of patients with essential hypertension showed that the cardiovascular disease hazard ratio for atenolol was 0.88, and the mortality hazard ratio was 0.99. Other meta-analyses have found similar results. A meta-analysis including over 145,000 patients suggested that the risk of stroke in patients taking atenolol may be related to patient age. Therefore, the use of atenolol may need to be based on more patient factors beyond hypertension. Atenolol is a beta-adrenergic blocker. Its mechanism of action is as an adrenergic beta receptor antagonist. Atenolol is a cardiac-selective beta-blocker widely used to treat hypertension and angina. Atenolol has been associated with rare cases of drug-induced liver injury, some of which are fatal. Atenolol is a synthetic isopropylaminopropanol derivative used as an antihypertensive, antihypertensive, and antiarrhythmic agent. Atenolol is a peripheral cardiac-selective beta-blocker that specifically acts on β1-adrenergic receptors and does not have intrinsic sympathomimetic effects. It can reduce exercise heart rate and slow atrioventricular conduction, thereby reducing overall oxygen consumption. (NCI04)
Atenolol is a so-called β1-selective (or “cardiac-selective”) drug. This means that it blocks β1 receptors in the heart muscle more strongly than it blocks β2 receptors in the lungs. β2 receptors are responsible for maintaining the patency of the bronchial system. If these receptors are blocked, it can lead to bronchospasm, resulting in severe hypoxia. However, because atenolol is cardiac-selective, the risk of bronchospasm is lower when using atenolol compared to non-selective drugs such as propranolol. Nevertheless, this reaction can still occur with atenolol, especially at high doses. Extra caution should be exercised when administering atenolol to asthmatic patients, as they are particularly susceptible to this reaction; the dose should be kept as low as possible. In case of an asthma attack, inhaled β2-receptor agonist antiasthmatic drugs, such as pentoxifylline or salbutamol, can usually suppress symptoms. Atenol (brand name: Tenormin) is used to treat cardiovascular diseases such as hypertension, coronary artery disease, and arrhythmias, as well as the treatment of acute myocardial infarction. Atenolol can be used in combination with other antihypertensive drugs in patients with compensated congestive heart failure (usually in combination with angiotensin-converting enzyme inhibitors, diuretics, and digitalis glycosides, if indicated). In patients with congestive heart failure, atenolol can reduce myocardial oxygen demand and consumption. Because atenolol also reduces myocardial contractility, it is important to start with a low dose, as this is an adverse reaction in patients with congestive heart failure.
A cardiac selective β1-adrenergic blocker with properties and potency similar to propranolol, but without negative inotropic effects.
See also: Atenolol; Chlorthalidone (component); Atenolol; Scopolamine hydrobromide (component).
Indications: 1) Treatment of hypertension, alone or in combination with other antihypertensive drugs. 2) Treatment of angina pectoris associated with coronary atherosclerosis. 3) Treatment of patients with acute myocardial infarction who are hemodynamically stable, have a heart rate greater than 50 beats/min, and a systolic blood pressure greater than 100 mmHg. Off-label use includes: 1) Secondary prevention of myocardial infarction. 2) Treatment of heart failure. 3) Treatment of atrial fibrillation. 4) Treatment of supraventricular tachycardia. 5) Treatment of ventricular arrhythmias, such as congenital long QT syndrome and arrhythmogenic right ventricular cardiomyopathy. 6) In combination with methimazole for the treatment of symptomatic thyrotoxicosis. 7) Prevention of migraines. 8) Treatment of alcohol withdrawal symptoms.
FDA Label

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Mechanism of Action
Atenolol is a cardiac selective beta-blocker. It is called a cardiac selective beta-blocker because it selectively binds to β1-adrenergic receptors, and its antagonistic ability has been reported to be 26 times higher than that of β2 receptors. Because β1 receptors are abundant in cardiac tissue, selective activity against β1 receptors results in cardiac selectivity. Binding to β2 receptors and possibly β3 receptors may still occur at therapeutic doses, but the effect of antagonizing these receptors is significantly reduced compared to non-selective drugs. β1 and β2 receptors are coupled to Gs proteins, so antagonizing their activation reduces the activity of adenylate cyclase and its downstream signaling via cyclic adenosine monophosphate and protein kinase A (PKA). In cardiomyocytes, PKA is thought to mediate the activation of L-type calcium channels and rennet receptors via phosphorylation. L-type calcium channels subsequently cause an initial increase in intracellular calcium ion concentration and trigger rennet receptors to release calcium ions stored in the sarcoplasmic reticulum (SR), thereby enhancing myocardial contractility. PKA also inhibits contractility by phosphorylating phosphoproteins, which in turn increase the affinity of SR Ca²⁺-ATPase, thereby increasing SR calcium ion reuptake. Furthermore, PKA phosphorylates troponin I to reduce its affinity for calcium ions. Both of these events lead to decreased myocardial contractility, which, combined with increased initial contractility, results in a faster circulatory rate, thus increasing heart rate and myocardial contractility. L-type calcium channels are also a major factor in myocardial depolarization; their activation can increase the frequency of action potentials and may increase the incidence of ectopic potentials. Similar inhibitory events occur in bronchial smooth muscle, mediating relaxation, including phosphorylation of myosin light chain kinase, thereby reducing its affinity for calcium. Protein kinase A (PKA) also inhibits excitatory Gq-coupled pathways by phosphorylating inositol triphosphate receptors and phospholipase C, thereby inhibiting intracellular calcium release. Therefore, antagonizing this activity with β-blockers like atenolol leads to increased bronchial contractility. Atenol produces negative chronotropic and negative inotropic effects by inhibiting myocardial β1-adrenergic receptors. Atenolol's negative chronotropic effect on the sinoatrial node leads to a decrease in the sinoatrial node's firing rate and a prolonged recovery time, thereby reducing heart rate at rest and during exercise, as well as reflex orthostatic tachycardia, by approximately 25-35%. High doses of atenolol may cause sinus arrest, especially in patients with sinoatrial node disease (e.g., sick sinus syndrome). Atenolol also slows atrioventricular conduction. Although the stroke index may moderately increase by about 10%, atenolol typically reduces cardiac output by about 20%, likely due to its effect on heart rate. The decrease in myocardial contractility, heart rate, and blood pressure caused by atenolol usually results in a reduction in myocardial oxygen consumption, explaining the drug's efficacy in chronic stable angina. However, atenolol can increase oxygen demand by increasing left ventricular fiber length and end-diastolic pressure, particularly in patients with heart failure. Atenolol inhibits plasma renin activity and the renin-aldosterone-angiotensin system. The toxic effects of β-blockers appear to be related to their membrane inhibitory activity and may be due to their action on β-adrenergic receptors, which are different 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.)