Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new atenolol research articles will be listed here shortly after becoming available to us.
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Medical research on atenolol
Anterior spinal cord syndrome after initiation of treatment with atenolol.
J Emerg Med. 2008 Jun 30;
Schneider GS
Anterior spinal cord syndrome is a rare condition with a variety of precipitating factors. Patients typically complain of weakness or paralysis of the extremities, often accompanied by pain, but frequently without a history of trauma. A 48-year-old man presented to the emergency department complaining of neck pain and inability to move his legs in the absence of trauma. Several hours prior he had seen his private physician and was given a dose of atenolol for elevated blood pressure. He had not previously been on medications for hypertension. His neurological examination revealed bilateral paralysis of the lower extremities. In the upper extremities he had weakness and sensory loss at the level of C6. Rectal tone was decreased and without sensation. Cervical and thoracic spine magnetic resonance imaging showed spondylotic disc disease, with disc herniation at C6-7 causing severe spinal canal stenosis. Despite i.v. methylprednisolone, pressors, and a prolonged intensive care unit course, the patient was discharged 5 weeks later with continued neurological deficits. Anterior spinal cord syndrome results from compression of the anterior spinal artery and often occurs in the absence of traumatic injury. The recognition, management, and prognosis of this condition are discussed. (c) 2008 Elsevier Inc.
J Neurosci. 2008 Jun 25; 28(26): 6642-51
Roozendaal B, Schelling G, McGaugh JL
Extensive evidence indicates that stress hormone effects on the consolidation of emotionally influenced memory involve noradrenergic activation of the basolateral complex of the amygdala (BLA). The present experiments examined whether corticotropin-releasing factor (CRF) modulates memory consolidation via an interaction with the beta-adrenoceptor-cAMP system in the BLA. In a first experiment, male Sprague Dawley rats received bilateral infusions of the CRF-binding protein ligand inhibitor CRF(6-33) into the BLA either alone or together with the CRF receptor antagonist alpha-helical CRF(9-41) immediately after inhibitory avoidance training. CRF(6-33) induced dose-dependent enhancement of 48 h retention latencies, which was blocked by coadministration of alpha-helical CRF(9-41), suggesting that CRF(6-33) enhances memory consolidation by displacing CRF from its binding protein, thereby increasing "free" endogenous CRF concentrations. In a second experiment, intra-BLA infusions of atenolol (beta-adrenoceptor antagonist) and Rp-cAMPS (cAMP inhibitor), but not prazosin (alpha(1)-adrenoceptor antagonist), blocked CRF(6-33)-induced retention enhancement. In a third experiment, the CRF receptor antagonist alpha-helical CRF(9-41) administered into the BLA immediately after training attenuated the dose-response effects of concurrent intra-BLA infusions of clenbuterol (beta-adrenoceptor agonist). In contrast, alpha-helical CRF(9-41) did not alter retention enhancement induced by posttraining intra-BLA infusions of either cirazoline (alpha(1)-adrenoceptor agonist) or 8-br-cAMP (cAMP analog). These findings suggest that CRF facilitates the memory-modulatory effects of noradrenergic stimulation in the BLA via an interaction with the beta-adrenoceptor-cAMP cascade, at a locus between the membrane-bound beta-adrenoceptor and the intracellular cAMP formation site. Moreover, consistent with evidence that glucocorticoids enhance memory consolidation via a similar interaction with the beta-adrenoceptor-cAMP cascade, a last experiment found that the CRF and glucocorticoid systems within the BLA interact in influencing beta-adrenoceptor-cAMP effects on memory consolidation.
Rev Med Liege. 2008 Apr; 63(4): 220-4
Lancellotti P
Ivabradine (Procoralan), a new If inhibitor which acts specifically and in a dose-dependent manner on the pacemaker activity of the sinoatrial node, is a pure heart rate lowering agent. It slows the diastolic depolarization slope of sinoatrial node cells and reduces heart rate at rest and during exercise. It has shown anti-ischaemic and anti-anginal activity at recommended doses of 5 and 7.5 mg bid in patients with stable angina. Ivabradine is as effective as atenolol and amlodipine to prevent or attenuate exercise-induced ischaemia in these patients. It is well tolerated, with transient visual symptoms being the main drug-related adverse event. These symptoms may be linked to the presence in the retina of ion channels similar to cardiac If channels and did not adversely affect the tolerability of the drug for most patients. In Belgium, ivabradine is currently reimbursed in patients with stable angina and normal sinus rhythm who do not tolerate beta-blockers and non-dihydropyridine calcium antagonists or in whom these treatments are contra-indicated.
Pharmacokinetic/pharmacodynamic modeling of the cardiovascular effects of beta blockers in humans.
Arch Pharm Res. 2008 Jun; 31(6): 814-21
Baek IH, Yun MH, Yun HY, Kwon KI
Pharmacokinetic-pharmacodynamic (PK/PD) analysis is useful study in clinical pharmacology, also PK/PD modeling is major tools for PK/PD analysis. In this study, we sought to characterize the relationship between the cardiovascular effects and plasma concentrations of the beta blocker drugs carvedilol and atenolol using PK/PD modeling in healthy humans. One group received oral doses of atenolol (50 mg) and the other group received oral doses of carvedilol (25 mg). Subsequently, blood samples were taken, and the effects of the drugs on blood pressure were determined. Plasma concentrations of drugs were measured by HPLC, and PK/PD modeling performed by applied biophase model, plasma drug concentrations were linked to the observed systolic blood pressure (SBP) and diastolic blood pressure (DBP) via an effect compartment. The model parameters were estimated using the ADAPT II program. In PK/PD analysis, it was observed the time delay between plasma concentration and effect and the time delay between SBP and DBP. The two time delays were properly explained by PD parameter "K ( eo )" in applied biophase model. As conclusion, the biophase PK/PD model described the relationship between the plasma concentrations of the drugs and the cardiovascular effects, including the time delay between systolic blood pressure and diastolic blood pressure.
Adv Ther. 2008 Jun; 25(6): 619-626
Tuncer M, Guntekin U, Gunes Y, Gumrukcuoglu HA, Eryonucu B
INTRODUCTION: Impaired left ventricular (LV) diastolic relaxation, detected by pulsed Doppler echocardiography, is predictive of a higher incidence of major cardiovascular events in hypertensive patients. An improvement in LV diastolic function is an important goal of treatment. However, treatment of LV diastolic dysfunction remains empirical. The objective of our study was to compare the short-term effects of nebivolol and atenolol on Doppler diastolic filling parameters in hypertensive patients. METHODS: A total of 32 patients with mild-to-moderate hypertension were enrolled in the study. The patients were randomly assigned to receive treatment with either nebivolol (5 mg/day) or atenolol (50 mg/day) for 1 month. Diastolic filling parameters, with pulsed-wave Doppler transmitral flow velocities, were measured 1 day before and 1 month after treatment. RESULTS: Compared with baseline, both agents significantly decreased heart rate and blood pressure. However, there was no significant difference in pre-and post-treatment values between the nebivolol and atenolol groups. Both drugs significantly improved LV transmitral flow measured by early diastolic flow/atrial contraction signal (E/A) ratio, decreased deceleration time (DT) and isovolumetric contraction time (IVRT), but post-treatment improvement in E/A, DT and IVRT values was more significant with nebivolol compared with atenolol (P=0.05, P=0.05 and P=0.003, respectively). CONCLUSIONS: Although treatment with nebivolol or atenolol results in improved LV transmitral diastolic function filling parameters (E/A ratio, IVRT and DT), nebivolol has a greater effect compared with atenolol in patients with mild-to-moderate hypertension.
Br J Pharmacol. 2008 Jun 16;
Ngala RA, O'Dowd J, Wang SJ, Agarwal A, Stocker C, Cawthorne MA, Arch JR
Background and purpose:Picomolar concentrations of the beta(3)-adrenoceptor agonist BRL37344 stimulate 2-deoxyglucose uptake in soleus muscle via undefined receptors. Higher concentrations alter uptake, apparently via beta(2)-adrenoceptors. Effects of BRL37344 and beta(2)-adrenoceptor agonists are compared.Experimental approach:Mouse soleus muscles were incubated with 2-deoxy[1-(14)C]-glucose, [1-(14)C]-palmitate or [2-(14)C]-pyruvate, and BRL37344, beta(2)-adrenoceptor agonists and selective beta-adrenoceptor antagonists. Formation of 2-deoxy[1-(14)C]-glucose-6-phosphate or (14)CO(2) was measured. 2-Deoxy[1-(14)C]-glucose uptake and beta-adrenoceptor mRNA were measured in C2C12 cells.Key results:10 pM BRL37344, 10 pM clenbuterol and 100 pM salbutamol stimulated 2-deoxyglucose uptake in soleus muscle by 33-54%. The effect of BRL37344 was prevented by 1 muM atenolol but not by 300 nM CGP20712A or IC3118551, or 1 muM SR59230A; that of clenbuterol was prevented by ICI118551 but not atenolol. 10 nM BRL37344 st4mulated 2-deoxyglucose uptake, whereas 100 nM clenbuterol and salbutamol inhibited uptake. These effects were blocked by ICI118551. Similar results were obtained in C2C12 cells, in which only beta(2)-adrenoceptor mRNA could be detected by RT-PCR. 10 nM BRL37344 and 10 pM clenbuterol stimulated muscle palmitate oxidation. In the presence of palmitate, BRL37344 no longer stimulated 2-deoxyglucose uptake and the effect of clenbuterol was not significant.Conclusions and implications:Stimulation of glucose uptake by 10 pM BRL37344 and clenbuterol involves different atypical pharmacologies. Nanomolar concentrations of BRL37344 and clenbuterol, probably acting via beta(2)-adrenoceptors, have opposite effects on glucose uptake. The agonists preferentially stimulate fat rather than carbohydrate oxidation, but stimulation of endogenous fat oxidation cannot explain why 100 nM clenbuterol inhibited 2-deoxyglucose uptake.British Journal of Pharmacology advance online publication, 16 June 2008; doi:10.1038/bjp.2008.244.
J Hypertens. 2008 Jul; 26(7): 1463-1471
Matsui Y, Eguchi K, Shibasaki S, Ishikawa J, Hoshide S, Pickering TG, Shimada K, Kario K,
OBJECTIVES: Doxazosin is reported to increase the incidence of congestive heart failure. The benefits of doxazosin, for controlling morning blood pressure as well as its effect on the left ventricular structure and function, are herein examined. METHODS: In this study, 223 morning hypertensive patients were randomized into either the doxazosin group, with a once-daily bedtime dose of doxazosin, or the control group, who continued their current medication. Atenolol was added to the doxazosin group when needed. The effect of doxazosin was evaluated by measurement of echocardiographic parameters and B-type natriuretic peptide. RESULTS: The left ventricular wall thickness decreased, but the left ventricular diastolic diameter in the doxazosin group increased from the baseline. The changes in the left ventricular mass index were similar between the groups, whereas the relative wall thickness in the doxazosin group decreased more than that in the control group. The left ventricular diastolic function could deteriorate in the doxazosin group. In the doxazosin group, an increase in the left ventricular diameter was only seen in the patient who did not take diuretics throughout the study. The office and home blood pressure in the doxazosin group decreased more than that in the control group, whereas the B-type natriuretic peptide increased in the doxazosin group. Three cases of congestive heart failure were observed in the doxazosin group, but none in the control group. CONCLUSION: Although a bedtime dose of doxazosin can significantly lower the blood pressure, it can also increase left ventricular diameter, thus increasing the risk of congestive heart failure. However, the prior use of diuretics can prevent the unfavorable effects of doxazosin on the left ventricular structure.
Olmesartan medoxomil : a review of its use in the management of hypertension.
Drugs. 2008; 68(9): 1239-72
Scott LJ, McCormack PL
Olmesartan medoxomil (Olmetec((R)), Benicar((R))) is an angiotensin II type 1 (AT(1)) receptor antagonist (angiotensin receptor blocker [ARB]) that inhibits the actions of angiotensin II on the renin-angiotensin-aldosterone system, which plays a key role in the pathogenesis of hypertension. Oral olmesartan medoxomil 10-40 mg once daily is recommended for the treatment of adult patients with hypertension. In those with inadequate BP control using monotherapy, fixed-dose olmesartan medoxomil/hydrochlorothiazide (HCTZ) [Olmetec plus((R)), Benicar-HCT((R))] combination therapy may be initiated.Extensive clinical evidence from several large well designed trials and the clinical practice setting has confirmed the antihypertensive efficacy and good tolerability profile of oral olmesartan medoxomil, as monotherapy or in combination with HCTZ, in patients with hypertension, including elderly patients with isolated systolic hypertension (ISH). Notably, BP control is sustained throughout the 24-hour dosage interval, including during the last 4 hours of this period. In clinical trials, olmesartan medoxomil monotherapy provided better antihypertensive efficacy than losartan, candesartan cilexetil or irbesartan monotherapy, and was at least as effective as valsartan treatment, with a faster onset of action than other ARBs in terms of reductions from baseline in diastolic BP (DBP) and, in most instances, systolic BP (SBP). Combination therapy with olmesartan medoxomil plus HCTZ was superior to that with benazepril plus amlodipine, as effective as that with losartan plus HCTZ, noninferior to that with atenolol plus HCTZ, but less effective than that with telmisartan plus HCTZ, in individual trials. Data from ongoing clinical outcome trials are required to more fully determine the relative position of olmesartan medoxomil therapy in the management of hypertension. In the meantime, the consistent antihypertensive efficacy during the entire 24-hour dosage interval and good tolerability profile of olmesartan medoxomil, with or without HCTZ, make it a valuable option for the treatment of adult patients with hypertension, including the elderly.
Kardiologiia. 2008; 48(5): 60-1
Tatarchenko IP, Pozdniakova NV, Biriuchenko MV
In vitro and in vivo transdermal studies of atenolol using iontophoresis.
Acta Pol Pharm. 2008 Jan-Feb; 65(1): 29-36
Inal O, Kiliçarslan M, Ari N, Baykara T
Matrix formulations of Eudragit E 100: NE 40D polymers (100:0, 70:30, 60:40, 50:50% w/w) with 20% w/w of triacetine and 5% w/w of atenolol were prepared by film casting method with different solvents (methanol, 2-propanol and acetone). In vitro release of atenolol from the films were studied by vertical Franz diffusion cells in HEPES buffer (pH 7.4) for 78 h. Direct currents of 0.1 and 0.5 mA/cm2 were applied for 6 h to the formulations with Ag/AgCl electrodes. Also, transdermal application for the Eudragit E 100: NE 40 D (70:30% w/w) formulation was compared by iontophoresis or oleic acid (2.5% w/v) with control group on Wistar rats. As a result, the in vitro release rate of atenolol from films were increased with iontophoresis by increasing the current density (from 0.240 to 0.424 mg/cm2 for 70:3% w/w formulation) and also increased with the amount of Eudragit NE 40D (from 0.646 to 1.30 mg/cm2 at the end of 78 h). It is obtained from the in vivo studies that oleic acid provided a higher plasma and skin concentration (0.825 mg/mL and 12.5 mg/cm2, respectively) than iontophoresis treatment (0.399 mg/mL and 1.81 mg/cm2, respectively) due to the different mechanisms. However, the results showed that iontophoresis is a good alternative for enhancing the transdermal delivery of atenolol.