Sotalol 0-antagonist

Ventricular extrasystoles are treated only if they may degenerate into life-threatening arrhythmia. In milder forms the proarrhythmic risk of the diugs overshadows their benefits. In such cases (3-adrenoceptor antagonists may be attempted. For the treatment of ventricular extrasystoles, such as series or runs of extrasystoles, amiodarone or sotalol are used. In the absence of structural heart disease, class I anti-arrhythmic diugs can be considered an alternative. However, they may not be administered during the post-infarction period. 

The bioslurry treatment successfully removed several of the PhC to non-detectable levels after 26 days three histamine H2-receptor antagonists (ranitidine, famotidine, cimetidine), two (1-blockers (atenolol, sotalol), one barbiturate (butalbital) and one antidiabetic compound (glibenclamide). The elimination of the sulfonamide antibiotics sulfapyridine (100%), sulfamethazine (91.0%) and... 

Similar to dihydropyridine calcium blockers, many 0-adrenoreceptor antagonists exhibit antioxidant activity. Mak and Weglinski [290] showed that the pretreatment of canine myocytic sarcolemmal membranes with 0-adrenoreceptor antagonists (propranolol, pindolol, metoprolol, atenolol, or sotalol) (Figure 29.15) inhibited superoxide-induced sarcolemmal... 

II Propranolol Metoprolol Nadolol Acebutolol Atenolol Pindolol Timolol Sotalol EsmoloF 3-Adrenoceptor antagonist, cardiac membrane stabilization, indirect effect on sinoatrial node to decrease rate of spontaneous diastolic depolarization. Indirect effect on A-V node to decrease conduction velocity and prolong ERR... 

The hemodynamic effects of sotalol are related to its 3-adrenoceptor antagonist activity. Accordingly, decreases in resting heart rate and in exercise-induced tachycardia are seen in patients receiving sotalol. A modest reduction in systolic pressure and in cardiac output may occur. The reduction in cardiac output is a consequence of lowering the heart rate, since stroke volume is unaffected by sotalol treatment. In patients with normal ventricular function, cardiac output is maintained despite the decrease in heart rate because of the simultaneous increase in the stroke volume. 

Ketanserin should not be combined with drugs that prolong the QT interval, e.g. class la anti-arrhythmics, amiodarone, sotalol, erythromycin. The risk of torsade de pointes secondary to hypokalaemia is increased when ketanserin is combined with thiazides or loop diuretics without concomitant use of a potassium-sparing diuretic or an angiotensin-converting enzyme (ACE) inhibitor, a 1 Antagonists... 

Local anesthetic action, also known as "membrane-stabilizing" action, is a prominent effect of several 3 blockers (Table 10-2). This action is the result of typical local anesthetic blockade of sodium channels (see Chapter 26) and can be demonstrated experimentally in isolated neurons, heart muscle, and skeletal muscle membrane. However, it is unlikely that this effect is important after systemic administration of these drugs, since the concentration in plasma usually achieved by these routes is too low for the anesthetic effects to be evident. These membrane-stabilizing 3 blockers are not used topically on the eye, where local anesthesia of the cornea would be highly undesirable. Sotalol is a nonselective 3-receptor antagonist that lacks local anesthetic action but has marked class III antiarrhythmic effects, reflecting potassium channel blockade (see Chapter 14). 

KCAs) are among the numerous classes of drugs developed to control hypertension. See also Enzyme Inhibitors. /(-Adrenoceptor antagonists exemplified hy the phenoxypropanolamine derivatives propranolol and alprenolol and or the phenethanolamine drugs such as sotalol and require for activity both the ethanolamine portion and an aromatic ring. Furthermore, the correct spatial arrangement of the phenyl, ethylamine, and hydroxyl moieties is critical for /1-blockade. 

In contrast, amiodarone and sotalol are effective in most supraventricular and ventricular tachycardias. Amiodarone displays electrophysiologic characteristics consistent with each type of antiarrhythmic drug, ft is a sodium channel blocker with relatively fast on-off kinetics, has nonselec-tive j8-blocking actions, blocks potassium channels, and has slight calcium antagonist activity. The impressive effectiveness and low proarrhythmic potential of amiodarone have challenged the notion that selective ion channel blockade is preferable. Sotalol is a potent inhibitor of outward... 

P-adrenoceptor antagonists are effective for a range of supraventricular arrhythmias, in particular those associated with exercise, emotion or hyperth5o oidism. Sotalol may be used to suppress ventricular ectopic beats and ventricular tachycardia possibly in conjimction with amiodarone. 

Lipid solubility (13) determines the extent to which a drug partitions between an organic solvent and water. Propranolol, oxprenolol, metoprolol, and timolol are the most lipid-soluble beta-adrenoceptor antagonists, and atenolol, nadolol, and sotalol are the most water-soluble acebutolol and pindolol are intermediate (14). 

It has been argued that drug combinations that contain a beta-adrenoceptor antagonist in combination with a thiazide diuretic minimize the hypokalemic effect of the latter however, marked hypokalemia in the absence of primary hyperaldosteronism has been reported in a patient taking Sotazide (a combination of hydrochlorothiazide and the non-selective drug sotalol) (204). The use of a combination formulation of chlortaUdone and atenolol has also produced hypokalemia (205), in one case complicated by ventricular fibrillation after myocardial infarction (206). 

The list of beta-adrenoceptor antagonists that have been detected in breast milk includes atenolol (322), acebutolol and its active A-acetyl metabolite (323), metoprolol (324), nadolol (325), oxprenolol and timolol (326), propranolol (327), and sotalol (328). Most authors have concluded that the estimated daily infant dose derived from breastfeeding is likely to be too low to produce untoward effects in the suckling infant, and indeed such effects were not noted in the above cases. However, in the case of... 

The bradycardia produced by digoxin can be enhanced by beta-adrenoceptor antagonists. Neostigmine enhances vagal activity and can aggravate bradycardia (410). An apparent interaction between sotalol and thiazide-induced hypokalemia, resulting in torsade de pointes (411), has prompted the withdrawal of the combination formulation Sotazide. 

Arrhythmias 3- Antagonists Reduce sinoatrial rate and atrioventricular conductance Propranolol, Sotalol... 

Beta-blockers, by inhibiting the effect of adrenaline and noradrenaline on the heart, prevent the normal increase in heart rate, and are very effective in preventing exercise angina. Examples of beta-blockers used for this purpose include acebutolol, atenolol, metoprolol. nadolol, oxprenolol, pindolol, propranolol, sotalol and timolol. See ADRENOCEPTOR ANTAGONISTS. 

Beta-blockers, of which there are many, may be used if further treatment is necessary, with or without simultaneous administration of a diuretic e.g. acebutolol, oxprenolot, propranolol and sotalol. See adrenoceptor antagonists. 

SOtalOl [ban, INN] (sotalol hydrochloride [usan] Sotacor ) is a (both class II and III) antiarrhythmic and (subtype-non-selective) -adrenoceptor antagonist, which is relatively water-soluble. Chemically, it is a racemate with the receptor-biocking activity residing in the (-)-isomer, and antiarrhythmic activity shown by both (the (-1-) -S-form is dexsotalol). Therapeutically, it is normally used as an antiarrhythmic rather than as an antihypertensive. sotalol hydrochloride sotalol. soterenol [inn] (soterenol hydrochloride [usan]) is a P-ADRENOCEPTOR AGONIST. Therapeutically, it can be used as a BRONCHODILATOR in ANTIASTHMATIC treatment. 

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