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Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
No human teratology or reproduction studies with betaxolol, carteolol, nadolol, penbutolol, or timolol have been published. No increase in congenital malformations was noted in the offspring of pregnant mice who received up to 150 mg/kg/day of carteolol (Tanaka et al., 1979). Only six infants were exposed to betaxolol during the first trimester in the Swedish Birth Defects Registry (Kallen, 2019). Also, no increase in the frequency of malformations was found among the offspring of rats, rabbits, and hamsters that had received nadolol in doses several times higher than the usual human dose (Sibley et al., 1978; Stevens et al., 1984). No increased frequency of adverse fetal effects was found in the offspring of mice treated with penbutolol (Sugisaki et al., 1981).
Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A patient sensitized to metipranolol was patch tested with a series of other beta-blockers and had a positive reaction only to l-penbutolol sulfate, to which she had most likely not been exposed before and consequently may represent a cross-reaction (6).
Pharmacokinetic-Pharmacodynamic Modeling of Reversible Drug Effects
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Brockmeier et al.47 measured the PK of penbutolol, a β-receptor antagonist, the reduction in exercise-induced tachycardia, and the in vitro inhibition of radioligand binding to β-adrenoreceptors on rat reticulocyte membranes by plasma in healthy normal volunteers. They could demonstrate a linear correlation between the PD effect and the in vitro inhibition of radioligand binding by plasma indicating that the reduction in exercise-induced tachycardia was mediated by the same β-receptors; the time course of the PD effect, E-t, could be explained completely by the in vitro inhibition of radioligand binding. However, plotting the reduction in tachycardia or the in vitro radioligand inhibition vs. cp (E-cp), both profiles showed significant time-related counterclockwise hysteresis, providing conclusive evidence for an (unknown) active metabolite that was competing with penbutolol for in vitro and in vivo binding sites, resulting in prolongation of the in vitro radioligand inhibition and the reduction in exercise tachycardia compared to cp of penbutolol.
Impact of chronic medications in the perioperative period: mechanisms of action and adverse drug effects (Part I)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Beta blockers exert their clinical effects through the inhibition of β-adrenergic receptors, with variable selectivity for β1, β2, and β3 sub-type receptors. β1-receptors are predominantly found in cardiac cells and produce positive chronotropic and ionotropic effects. These receptors are also located in renal cells and can induce production and release of renin. When β-blockers inhibit these receptors, they typically produce a decrease in heart rate, cardiac contractility, and blood pressure. In addition, cardiac oxygen demand is significantly decreased when β-receptors are inhibited [6]. Most beta-blockers are metabolized by the P450 enzyme system; however, atenolol and nadolol are excreted unchanged in the urine. The CYP1A2 and CYP2D6 enzyme systems are responsible for the propranolol biotransformation. Nonselective beta blockers block both beta-1 and beta-2 receptors (e.g. propranolol, nadolol, timolol maleate, penbutolol sulfate, sotalol hydrochloride, and pindolol), while cardio-selective beta blockers block only the Beta1 receptors (e.g. metoprolol, bisoprolol, atenolol, acebutolol, esmolol, and betaxolol) [7]. β-blockers are commonly used to treat cardiovascular conditions such as tachycardia, coronary artery disease, myocardial infarction, arrhythmias, hypertension, and aortic dissection. Nonselective β-blockers can affect other subtypes of β-receptors in other organ systems to treat other conditions such as glaucoma, migraines, and essential tremors [8]. Beta blockers are also used as adjuvants to treat anxiety, depression, mood disorders, acute stress/post-traumatic stress disorder, aggression, agitation, psychotic disorders, intellectual disability, and extrapyramidal symptoms. The lipophilic β-adrenergic blockers (e.g. metoprolol, propranolol, pindolol, timolol, and carvedilol) can cross the blood-brain barrier and produce neuropsychiatric effects (e.g. sleep disturbances). The hydrophilic β-blockers (e.g. atenolol and sotalol) cannot cross the blood-brain barrier and are devoid of neuropsychiatric side effects [9]. Lipophilic (vs. hydrophilic) β-blockers significantly reduce the risk of cardiovascular mortality and strokes in patients aged <65 years and ”all-cause mortality” in patients with coronary heart disease [10].
Elevated asleep blood pressure and non-dipper 24h patterning best predict risk for heart failure that can be averted by bedtime hypertension chronotherapy: A review of the published literature
Published in Chronobiology International, 2023
Ramón C. Hermida, Artemio Mojón, José R. Fernández, Ramón G. Hermida-Ayala, Juan J. Crespo, María T. Ríos, Manuel Domínguez-Sardiña, Alfonso Otero, Michael H. Smolensky
A total of 25 of the 29 (86.2%) trials entailing angiotensin-converting enzyme inhibitor (ACEI) medications of different terminal half-life – benazepril, captopril, enalapril, imidapril, lisinopril, perindopril, quinapril, ramipril, spirapril, trandolapril, and zofenopril – when routinely ingested at-bedtime/evening vs. upon-waking/morning reported significantly better: (i) attenuated asleep SBP mean without compromised effect on the awake or 24 h SBP means; (ii) normalization of the 24 h SBP dipper profile; and (iii) patient tolerance to treatment, i.e., decreased incidence of adverse effects. It is noteworthy that no single case of sleep-time hypotension was reported with bedtime/evening treatment. Similar significant ingestion-time differences in therapeutic effects, also independent of medication terminal half-life, were substantiated for most (19 out of 25; 76.0%) of the angiotensin-II receptor blocker (ARB) medication trials that involved candesartan, irbesartan, olmesartan, telmisartan, or valsartan. Again, not a single case of sleep-time hypotension was reported with the bedtime/evening ARB treatment. Moreover, bedtime ARB dosing significantly decreased urinary albumin excretion (UAE) in an amount strongly correlated with the extent of the reduction of the asleep SBP mean and increase of the sleep-time relative SBP decline, and additionally this treatment-time schedule increased eGFR, decreased renal vascular resistance, and reduced carotid artery plaque size. Some 30 out of the 41 published calcium-channel blockers (CCB) trials (73.2%) that investigated ingestion-time dependent effects of altiazem, amlodipine, barnidipine, cilnidipine, diltiazem, isradipine, nifedipine, nisoldipine, nitrendipine, and verapamil reported significantly greater reduced asleep SBP mean, increased dipping, decreased left ventricular mass, and/or improved safety – mainly significantly decreased risk of peripheral edema – with bedtime/evening treatment. The BP-lowering effect of various other hypertension medications – α-blocker doxazosin; ß-blockers bisoprolol, carvedilol, nebivolol, penbutolol, and propanolol; diuretics hydrochlorothiazide (HCTZ) and torasemide; plus methyldopa, guanabenz, and clonidine – additionally were reported to differ significantly according to their ingestion-time. Publications entailing these medications generally reported a more prolonged BP-lowering effect and a more profound asleep BP decrease when ingested at bedtime/evening than upon-waking/morning, and without significant ingestion-time differences in adverse effects (Hermida et al. 2021a).