beta(1)-adrenergic antagonists improve sleep and behavioural disturbances in a circadian disorder, Smith-Magenis syndrome. (1/69)Smith-Magenis syndrome (SMS) is a clinically recognisable contiguous gene syndrome ascribed to interstitial deletions of chromosome 17p11.2. Patients have a phase shift of their circadian rhythm of melatonin with a paradoxical diurnal secretion of the hormone. Serum melatonin levels and day-night behaviour were studied in nine SMS children (aged 4 to 17 years) given acebutolol, a selective beta(1)-adrenergic antagonist (10 mg/kg early in the morning). Cardiac examination, serum melatonin, motor activity recordings, and sleep diaries were monitored before and after drug administration. The present study shows that a single morning dose of acebutolol suppressed the inappropriate secretion of melatonin in SMS. A significant improvement of inappropriate behaviour with increased concentration, delayed sleep onset, increased hours of sleep, and delayed waking were also noted. These results suggest that beta(1)-adrenergic antagonists help to manage hyperactivity, enhance cognitive performance, and reduce sleep disorders in SMS. (+info)
Streptococcus pneumoniae PstS production is phosphate responsive and enhanced during growth in the murine peritoneal cavity. (2/69)Differential display-PCR (DDPCR) was used to identify a Streptococcus pneumoniae gene with enhanced transcription during growth in the murine peritoneal cavity. Northern dot blot analysis and comparative densitometry confirmed a 1.8-fold increase in expression of the encoded sequence following murine peritoneal culture (MPC) versus laboratory culture or control culture (CC). Sequencing and basic local alignment search tool analysis identified the DDPCR fragment as pstS, the phosphate-binding protein of a high-affinity phosphate uptake system. PCR amplification of the complete pstS gene followed by restriction analysis and sequencing suggests a high level of conservation between strains and serotypes. Quantitative immunodot blotting using antiserum to recombinant PstS (rPstS) demonstrated an approximately twofold increase in PstS production during MPC from that during CCs, a finding consistent with the low levels of phosphate observed in the peritoneum. Moreover, immunodot blot and Northern analysis demonstrated phosphate-dependent production of PstS in six of seven strains examined. These results identify pstS expression as responsive to the MPC environment and extracellular phosphate concentrations. Presently, it remains unclear if phosphate concentrations in vivo contribute to the regulation of pstS. Finally, polyclonal antiserum to rPstS did not inhibit growth of the pneumococcus in vitro, suggesting that antibodies do not block phosphate uptake; moreover, vaccination of mice with rPstS did not protect against intraperitoneal challenge as assessed by the 50% lethal dose. (+info)
Evidence towards the role of arylamine N-acetyltransferase in Mycobacterium smegmatis and development of a specific antiserum against the homologous enzyme of Mycobacterium tuberculosis. (3/69)Arylamine N-acetyltransferase (NAT) in humans inactivates the anti-tubercular drug isoniazid (INH). Homologues of human NAT are present in Mycobacterium tuberculosis and Mycobacterium smegmatis, where they can acetylate, and hence inactivate, INH. The in vivo role of mycobacterial NAT is not known but heterologous expression of the M. tuberculosis gene increases the INH resistance. The 0.85 kb nat gene is part of a gene cluster in M. smegmatis. The gene is transcribed as a large, 7.5 kb mRNA as demonstrated by Northern analysis. A nat knockout strain of M. smegmatis was generated by targeted disruption. The new strain was confirmed to be devoid of NAT activity. The growth of the knockout strain is considerably delayed compared with the wild-type, due to an extended lag phase. The knockout mutant has an increased sensitivity to INH as would be predicted. The NATs from M. smegmatis and M. tuberculosis have a high degree of homology, except in the region of the C terminus. A specific polyclonal antiserum raised against recombinant NAT protein from M. tuberculosis is described that recognizes a stretch of about twenty residues within the C terminus of M. tuberculosis NAT. This highly specific antiserum will enable comparison of nat expression between isolates of M. tuberculosis. (+info)
Plasma levels and beta-adrenoceptor blockade with acebutolol, practolol and propranolol in man. (4/69)1 The degree of beta-adrenoceptor blockade of isoprenaline-induced tachycardia has been determined in three healthy volunteers after the administration of single oral doses of acebutolol, practolol or propranolol. 2 Plasma levels of these drugs were determined either colorimetrically (acebutolol and practolol) or fluorimetrically (propranolol). The colorimetric assay of acebutolol in plasma is fully described but the other drugs were assayed by published methods. 3 The degree of beta-adrenoceptor blockade and the plasma level for acebutolol and practolol were well correlated, whereas in the case of propranolol correlation was poor, due in part to the presence in plasma of active metabolites not detected by the fluorimetric assay. The plasma levels of practolol and propranolol are in agreement with those previously reported. 4 The maximum cardiac beta-adrenoceptor blockade achieved in this study with the respective single oral doses of acebutolol (300 mg), practolol (400 mg) or propranolol (40 mg) were similar in each of the three subjects. Therefore the beta-adrenoceptor blocking potencies of these drugs against isoprenaline-induced tachycardia are inversely related to these doses; indicating that propranolol is 7-8 times more potent than acebutolol and the latter slightly more potent than practolol. (+info)
Comparison of the actions of acebutolol, practolol and propranolol on calcium transport by heart microsomes and mitochondria. (5/69)1 The effects of acebutolol, practolol and propranolol (0,5-3 mM) on calcium uptake, calcium binding and ATPase activities of the rabbit and rat heart microsomal and mitochondrial fractions were investigated. 2 Dose-response and time course experiments revealed that propranolol greatly inhibited microsomal and mitochondrial calcium uptake whereas both acebutolol and practolol showed slight depressant effects. 3 The ATPase activities of microsomal and mitochondrial fractions were decreased by acebutolol, practolol and propranolol; however, the latter agent was more effective than the other two. 4 The inhibitory effects of acebutolol, practolol and propranolol on mitochondria and microsomes were not antagonized by adrenaline. 5 Propranolol decreased calcium binding by the microsomal fraction only, whereas acebutolol and practolol had no effect on microsomal or mitochondrial calcium binding. 6 The sensitivity of the rabbit heart subcellular fractions to the beta-adrenoceptor blocking drugs was similar to that of the rat heart; however, the calcium uptake and ATPase activities of microsomes were more sensitive to propranolol than mitochondria in both species. 7 Perfusion of rat hearts with 0.2-1 mM propranolol decreased contractile force, and microsomal and mitochondrial fractions obtained from these hearts accummulated less calcium in comparison to the control. On the other hand, acebutolol and practolol (0.2-1nM) had no appreciable effects on contractile force or subcellular fractions under similar conditions. 8 The negative inotropic effect of propranolol may partly be due to its inhibitory actions on calcium transport by subcellular organelles of the myocardium; the depressant action of propranolol on calcium transport is unlikely to be due to its beta-adrenoceptor blocking property. (+info)
Nodal and BMP2/4 signaling organizes the oral-aboral axis of the sea urchin embryo. (6/69)In the sea urchin embryo, the oral-aboral axis is specified after fertilization by mechanisms that are largely unknown. We report that early sea urchin embryos express Nodal and Antivin in the presumptive oral ectoderm and demonstrate that these genes control formation of the oral-aboral axis. Overexpression of nodal converted the whole ectoderm into oral ectoderm and induced ectopic expression of the orally expressed genes goosecoid, brachyury, BMP2/4, and antivin. Conversely, when the function of Nodal was blocked, by injection of an antisense Morpholino oligonucleotide or by injection of antivin mRNA, neither the oral nor the aboral ectoderm were specified. Injection of nodal mRNA into Nodal-deficient embryos induced an oral-aboral axis in a largely non-cell-autonomous manner. These observations suggest that the mechanisms responsible for patterning the oral-aboral axis of the sea urchin embryo may share similarities with mechanisms that pattern the dorsoventral axis of other deuterostomes. (+info)
Effects of grapefruit juice on the pharmacokinetics of acebutolol. (7/69)AIMS: We aimed to investigate effects of grapefruit juice on acebutolol pharmacokinetics. METHODS: In a randomized cross-over study, 10 healthy subjects ingested 200 mL grapefruit juice or water three times daily for 3 days and twice on day 4. On day 3, each subject ingested 400 mg acebutolol with grapefruit juice or water. The concentrations of acebutolol and its metabolite diacetolol were measured in plasma and urine up to 33 h. RESULTS: Grapefruit juice decreased the peak plasma concentration (Cmax) of acebutolol by 19% from 872 +/- 207 ng mL(-1) to 706 +/- 140 ng mL(-1) (95% CI on the difference -306, -26.4; P < 0.05), and the area under the concentration time curve (AUC(0-33 h)) by 7%, from 4498 +/- 939 ng mL(-1) h to 4182 +/- 915 ng mL(-1) h (95% CI -609, -23.0; P < 0.05). The half-life (t1/2) of acebutolol prolonged from 4.0 to 5.1 h (P < 0.05). The time to peak concentration and the amount of acebutolol excreted into urine (Ae) were unchanged. The Cmax, AUC(0-33 h), and Ae of diacetolol were decreased by 24% (P < 0.05), 18% (P < 0.05), and 20% (P < 0.01), respectively, by grapefruit juice. CONCLUSION: Grapefruit juice caused a small decrease in the plasma concentrations of acebutolol and diacetolol by interfering with gastrointestinal absorption. The interaction between the grapefruit juice and acebutolol is unlikely to be of clinical significance in most of the patients. (+info)
Transport of acebutolol through rabbit corneal epithelium. (8/69)The purpose of this study is to characterize transport of acebutolol through the corneal epithelium. Cultured normal rabbit corneal epithelial cells (RCEC) were used to investigate the drug transport. Primary RCEC were seeded on a filter membrane of Transwell-COL insert coated with fibronectin and were grown in Dulbecco's modified Eagle's medium/nutrient mixture F-12 with various supplements. Measurements of acebutolol permeability through RCEC layer were carried out to assess transcellular permeability coefficient (P(transcell)) in the absence or presence of inhibitors. Paracellular permeability coefficient (P(paracell)) was calculated by permeability coefficient of hydrophilic drugs (P(cell)). The transcellular permeability of acebutolol from apical side to basal side (A-to-B) showed concentration-dependency. The acebutolol flux in the A-to-B direction was smaller than that of opposite direction. Sodium azide, verapamil, and cyclosporin A enhanced the transcellular permeability of acebutolol in the A-to-B direction. Acebutolol permeability through an excised rabbit cornea was also increased by verapamil. Thus, it was suggested that acebutolol was actively secreted via P-glycoprotein in a corneal epithelium. (+info)
Acebutolol is a beta-adrenergic receptor blocker medication that is used to treat high blood pressure, angina (chest pain), and certain heart rhythm disorders. It works by blocking the effects of adrenaline on the heart, which can help to lower blood pressure and reduce the workload on the heart. Acebutolol is available in both immediate-release and extended-release forms, and it is typically taken orally. It is generally well-tolerated, but like all medications, it can cause side effects, such as dizziness, fatigue, and upset stomach.
Practolol is a non-selective beta-blocker medication that was once commonly used to treat high blood pressure, angina, and other cardiovascular conditions. It works by blocking the effects of adrenaline and other stress hormones on the heart, which can help to lower blood pressure and reduce the workload on the heart. Practolol is no longer widely used due to the development of more effective and safer beta-blockers. It has been associated with a number of side effects, including fatigue, dizziness, and bradycardia (slowed heart rate). In addition, it can interact with other medications and may not be suitable for everyone. As with any medication, the use of practolol should be carefully considered and monitored by a healthcare professional.
Propranolol is a medication that belongs to a class of drugs called beta blockers. It is primarily used to treat high blood pressure, angina (chest pain), and certain types of tremors, including essential tremor and tremors caused by medications. Propranolol can also be used to treat other conditions, such as anxiety disorders, certain types of heart rhythm disorders, and migraine headaches. It works by blocking the effects of adrenaline (a hormone that can cause the heart to beat faster and the blood vessels to narrow) on the heart and blood vessels. Propranolol is available in both oral and injectable forms, and it is usually taken once or twice a day.
17-Ketosteroids are a group of hormones that are produced by the adrenal glands and gonads. They are a type of steroid hormone that are derived from cholesterol and are involved in a variety of physiological processes in the body, including the regulation of metabolism, blood pressure, and the development and function of sexual characteristics. There are several different types of 17-ketosteroids, including cortisol, aldosterone, and androgens such as testosterone and dihydrotestosterone. These hormones are produced in different amounts by different organs and tissues in the body, and they have different effects on various physiological processes. In the medical field, 17-ketosteroids are often measured in blood or urine as a way to diagnose and monitor various medical conditions, such as Cushing's syndrome, Addison's disease, and certain types of cancer. They may also be used as a diagnostic tool to help identify the cause of certain symptoms or to monitor the effectiveness of certain treatments.
Dihydralazine is a medication that is used to treat high blood pressure (hypertension) and heart failure. It is a type of drug called a dihydropyridine calcium channel blocker, which works by relaxing blood vessels and allowing blood to flow more easily. This helps to lower blood pressure and improve the function of the heart. Dihydralazine is usually taken by mouth, but it can also be given as an injection. It is important to follow the instructions of your healthcare provider when taking this medication. Side effects of dihydralazine may include headache, dizziness, and nausea.
Adrenergic beta-antagonists are a class of drugs that block the action of adrenaline (epinephrine) and noradrenaline (norepinephrine) on beta-adrenergic receptors in the body. These receptors are found in various organs and tissues, including the heart, lungs, and blood vessels. When adrenaline and noradrenaline bind to beta-adrenergic receptors, they cause a number of physiological responses, such as increased heart rate, blood pressure, and bronchodilation. Adrenergic beta-antagonists work by blocking these receptors, thereby reducing the effects of adrenaline and noradrenaline. Adrenergic beta-antagonists are used to treat a variety of medical conditions, including high blood pressure, angina pectoris (chest pain), heart failure, and arrhythmias. They are also used to prevent migraines and to treat anxiety and panic disorders. Some common examples of adrenergic beta-antagonists include propranolol, atenolol, and metoprolol.
"Citrus paradisi" is the scientific name for the common grapefruit. In the medical field, grapefruit is known for its potential interactions with certain medications. Grapefruit contains compounds that can interfere with the metabolism of certain drugs, leading to increased levels of the drug in the bloodstream and potentially causing harmful side effects. As a result, healthcare providers may advise patients to avoid consuming grapefruit or grapefruit juice while taking certain medications.
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DeCS 2018 - July 31, 2018 version
Code System Concept
- Acebutolol (Sectral) Acebutolol is moved by pumps in cells in the body. (nih.gov)
- Acebutolol HCl capsules, USP are provided in two dosage strengths which contain 200 mg or 400 mg of acebutolol as the hydrochloride salt. (nih.gov)
- ISA has been observed with acebutolol in man, as shown by a slightly smaller (about 3 beats per minute) decrease in resting heart rate when compared to equivalent β-blocking doses of propranolol, metoprolol or atenolol. (nih.gov)
- The antihypertensive effect of acebutolol has been shown in double-blind controlled studies to be superior to placebo and similar to propranolol and hydrochlorothiazide. (nih.gov)
- The antiarrhythmic effect of acebutolol was compared with placebo, propranolol, and quinidine. (nih.gov)
- Both acebutolol and propranolol significantly reduced mean total and paired VEB and VT. (nih.gov)
- Glucose and lipid metabolism during acebutolol and propranolol therapy of angina in nondiabetic patients. (nih.gov)
Dose of acebutolol2
Allergic to acebutolol1
- tell your doctor and pharmacist if you are allergic to acebutolol, any other medications, or any ingredients in acebutolol capsules. (medlineplus.gov)
- Acebutolol is a cardioselective beta-blocker used in the treatment of hypertension, angina pectoris and cardiac arrhythmias. (nih.gov)
- acebutolol and atenolol both increase anti-hypertensive channel blocking. (medscape.com)
- acebutolol and nadolol both increase anti-hypertensive channel blocking. (medscape.com)
- acebutolol and penbutolol both increase anti-hypertensive channel blocking. (medscape.com)
- Bronchial Effects: In single-dose studies in asthmatics examining effects of various beta- blockers on pulmonary function, low doses of acebutolol produce less evidence of bronchoconstriction and less reduction of beta2 agonist, bronchodilating effects, than nonselective agents like propranolol but more than atenolol. (nih.gov)
- Pulmonary effects of acebutolol, a "cardioselective" beta adrenergic blocking agent. (nih.gov)
- Acebutolol overdose resulting in fatalities. (wikitox.org)
- Acebutolol comes as a capsule to take by mouth. (medlineplus.gov)
- Acebutolol also is used to treat certain irregular heart rhythms. (medlineplus.gov)
- If you suddenly stop taking acebutolol, you may experience serious heart problems such as angina (chest pain), heart attack, or an irregular heartbeat. (medlineplus.gov)
- Acebutolol is used to treat high blood pressure and irregular heartbeat (arrhythmia). (blinkhealth.com)
- The membrane-stabilizing effect of acebutolol is not manifest at the doses used clinically. (nih.gov)
- Acebutolol is also used sometimes to treat chest pain (angina). (medlineplus.gov)
- Acebutolol HCl, USP is a selective, hydrophilic beta-adrenoreceptor blocking agent with mild intrinsic sympathomimetic activity for use in treating patients with hypertension and ventricular arrhythmias. (nih.gov)
- Acebutolol is a cardio selective, β-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. (nih.gov)
Treat high blood pr1
- Acebutolol is used alone or in combination with other medications to treat high blood pressure. (medlineplus.gov)
- tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, nutritional supplements, and herbal products you are taking while you are taking acebutolol. (medlineplus.gov)
- The following nonprescription or herbal products may interact with acebutolol: nasal decongestants such as oxymetazoline (Afrin, Neo-Synephrine, Vicks Sinex, others) or cough and cold combination products that contain phenylephrine or pseudoephedrine. (medlineplus.gov)
- Acebutolol is in a class of medications called beta blockers. (medlineplus.gov)
- Be sure to let your doctor and pharmacist know that you are taking these medications before you start taking acebutolol. (medlineplus.gov)
- Do not start any of these medications while taking acebutolol without discussing with your healthcare provider. (medlineplus.gov)
- Acebutolol belongs to the class of medications called beta-blockers . (mediresource.com)
- A membrane-stabilizing effect has been detected in animals, but only with high concentrations of acebutolol. (nih.gov)
- In addition, patients responding to acebutolol administered twice daily had a similar response whether the dosage regimen was changed to once daily administration or continued on a b.i.d. regimen. (nih.gov)
- Vascular Effects: Acebutolol has less antagonistic effects on peripheral vascular β2-receptors at rest and after epinephrine stimulation than nonselective β-antagonists. (nih.gov)
- Significant reductions in resting and exercise heart rates and systolic blood pressures have been observed 1.5 hours after acebutolol administration with maximal effects occurring between 3 and 8 hours post-dosing in normal volunteers. (nih.gov)
- you should know that acebutolol may increase the risk of hypoglycemia (low blood sugar) and prevent the warning signs and symptoms that would tell you that your blood sugar is low. (medlineplus.gov)
- Acebutolol has been shown to delay AV conduction time and to increase the refractoriness of the AV node without significantly affecting sinus node recovery time, atrial refractory period, or the HV conduction time. (nih.gov)
- acebutolol and nebivolol both increase anti-hypertensive channel blocking. (medscape.com)
- There are significant correlations between plasma levels of acebutolol and both the reduction in resting heart rate and the percent of β-blockade of exercise-induced tachycardia. (nih.gov)
- For brands that may still be available, search under acebutolol. (mediresource.com)
- ISA of acebutolol has been demonstrated in catecholamine-depleted rats by tachycardia induced by intravenous administration of this agent. (nih.gov)