Analysis of information sources in references of the Wikipedia article "Atenolol" in English language version.
Interestingly, in one study, orthostatic hypotension was eliminated in a group of 61 patients treated for migraine headaches with phenelzine, when a beta-blocker, atenolol, was added (15). The authors have reported that hypertensive reactions were also less frequent when the two drugs were combined. We need further experience with this combination to determine whether addition of a beta-blocker is a safe and an effective strategy for alleviation of postural hypotension in depressed patients receiving an MAOI.
Atenolol is only minimally, if at all, metabolized and renally excreted in mostly unchanged form; thus an interaction with drugs that interfere with the hepatic metabolism is not to be expected. It is also very unlikely that the genetic polymorphisms of the CYP-family might affect the pharmacokinetics of atenolol. In fact it has been shown that plasma concentrations of nonmetabolized atenolol was not significantly different between "extensive" and "poor debrisoquine metabolizers" – in contrast to the plasma concentrations of metoprolol that were significantly increased in "poor metabolizers" (Dayer et al. 1985, Lewis et al. 1985). Furthermore, in healthy volunteers cimetidine (CAS 70059- 30-2) did not affect plasma concentrations of atenolol but significantly increased plasma concentrations of metoprolol or propranolol (Kirch et al. 1981).
Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people [...] Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3)
β-Blockers still represent widely prescribed drugs as they cover a wide spectrum of CV indications. Obviously, it is not trivial which β-blocker to choose as they differ both with regard to their PD and PK profiles [82]. It is well known when comparing the characteristics of atenolol, bisoprolol, metoprolol (each β-1 selective) and carvedilol (β-1 and β-2 nonselective). Among these β-blockers, atenolol is mainly eliminated by renal excretion; bisoprolol is in part excreted as parent compound via the renal route (50%); the other 50% are hepatically metabolized; whereas metoprolol and carvedilol are metabolized by CYP2D6. DDIs are mainly observed with those β-blockers that are metabolized via CYP enzymes. However, it should be emphasized that, in general, β-blockers are well-tolerated safe drugs with a large therapeutic index [83].
Amphetamines (Adderall, Dexedrine): Electrophysiological Effects of Amphetamines: Amphetamines have been associated with tachyarrhythmias and sudden death.113–115 Many of the electrophysiological effects of amphetamines may be initiated by the release of norepinephrine stores from presynaptic vesicles and blocking of norepinephrine reuptake.116,117 In addition, amphetamines are potent blockers of dopamine uptake and strong central nervous system stimulants. Dopaminergic Effects of Amphetamines: In addition to the β-agonist effects of amphetamines, the dopamine receptors D1 and D2 contribute to the cardiovascular effects of methamphetamine by producing a pressor response accounting for the increase in blood pressure. The D1 receptor also is involved in mediating the positive tachycardic effects of methamphetamine.117
Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na+ or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (Merikangas & Merikangas, 1995).
Atenolol is only minimally, if at all, metabolized and renally excreted in mostly unchanged form; thus an interaction with drugs that interfere with the hepatic metabolism is not to be expected. It is also very unlikely that the genetic polymorphisms of the CYP-family might affect the pharmacokinetics of atenolol. In fact it has been shown that plasma concentrations of nonmetabolized atenolol was not significantly different between "extensive" and "poor debrisoquine metabolizers" – in contrast to the plasma concentrations of metoprolol that were significantly increased in "poor metabolizers" (Dayer et al. 1985, Lewis et al. 1985). Furthermore, in healthy volunteers cimetidine (CAS 70059- 30-2) did not affect plasma concentrations of atenolol but significantly increased plasma concentrations of metoprolol or propranolol (Kirch et al. 1981).
Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people [...] Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3)
β-Blockers still represent widely prescribed drugs as they cover a wide spectrum of CV indications. Obviously, it is not trivial which β-blocker to choose as they differ both with regard to their PD and PK profiles [82]. It is well known when comparing the characteristics of atenolol, bisoprolol, metoprolol (each β-1 selective) and carvedilol (β-1 and β-2 nonselective). Among these β-blockers, atenolol is mainly eliminated by renal excretion; bisoprolol is in part excreted as parent compound via the renal route (50%); the other 50% are hepatically metabolized; whereas metoprolol and carvedilol are metabolized by CYP2D6. DDIs are mainly observed with those β-blockers that are metabolized via CYP enzymes. However, it should be emphasized that, in general, β-blockers are well-tolerated safe drugs with a large therapeutic index [83].
Amphetamines (Adderall, Dexedrine): Electrophysiological Effects of Amphetamines: Amphetamines have been associated with tachyarrhythmias and sudden death.113–115 Many of the electrophysiological effects of amphetamines may be initiated by the release of norepinephrine stores from presynaptic vesicles and blocking of norepinephrine reuptake.116,117 In addition, amphetamines are potent blockers of dopamine uptake and strong central nervous system stimulants. Dopaminergic Effects of Amphetamines: In addition to the β-agonist effects of amphetamines, the dopamine receptors D1 and D2 contribute to the cardiovascular effects of methamphetamine by producing a pressor response accounting for the increase in blood pressure. The D1 receptor also is involved in mediating the positive tachycardic effects of methamphetamine.117
Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people [...] Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3)
Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na+ or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (Merikangas & Merikangas, 1995).
