ISOPTIN® SR (verapamil hydrochloride) is a calcium ion influx inhibitor (slow channel blocker or calcium ion antagonist).
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Isoptin SR 120 mg
Isoptin SR 120 mg
Isoptin SR 120 mg
$85.68 USD + Bonus - 6 pills
Isoptin SR 120 mg
$110.88 USD + Bonus - 6 pills
ISOPTIN® SR (verapamil hydrochloride) is a calcium ion influx inhibitor (slow channel blocker or calcium ion antagonist). Isoptin SR is available for oral administration as light green, capsule shaped, scored, film-coated tablets containing 240 mg verapamil hydrochloride, as light pink, oval shaped, scored, film-coated tablets containing 180 mg verapamil hydrochloride, and as light violet, oval shaped, film-coated tablets containing 120 mg verapamil hydrochloride. The tablets are designed for sustained release of the drug in the gastrointestinal tract, sustained release characteristics are not altered when the tablet is divided in half.
Isoptin SR - Clinical Pharmacology
ISOPTIN (verapamil HCl) is a calcium ion influx inhibitor (slow channel blocker or calcium ion antagonist) that exerts its pharmacologic effects by modulating the influx of ionic calcium across the cell membrane of the arterial smooth muscle as well as in conductile and contractile myocardial cells.
Mechanism of Action
ISOPTIN exerts antihypertensive effects by decreasing systemic vascular resistance, usually without orthostatic decreases in blood pressure or reflex tachycardia; bradycardia (rate less than 50 beats/min) is uncommon (1.4%). During isometric or dynamic exercise ISOPTIN does not alter systolic cardiac function in patients with normal ventricular function. ISOPTIN does not alter total serum calcium levels. However, one report suggested that calcium levels above the normal range may alter the therapeutic effect of ISOPTIN.
Other Pharmacological Actions of ISOPTIN Include the Following
ISOPTIN (verapamil HCI) dilates the main coronary arteries and coronary arterioles, both in normal and ischemic regions, and is a potent inhibitor of coronary artery spasm, whether spontaneous or ergonovine-induced. This property increases myocardial oxygen delivery in patients with coronary artery spasm, and is responsible for the effectiveness of ISOPTIN in vasospastic (Prinzmetal’s or variant) as well as unstable angina at rest. Whether this effect plays any role in classical effort angina is not clear, but studies of exercise tolerance have not shown an increase in the maximum exercise rate-pressure product, a widely accepted measure of oxygen utilization. This suggests that, in general, relief of spasm or dilation of coronary arteries is not an important factor in classical angina.
ISOPTIN regularly reduces the total systemic resistance (afterload) against which the heart works both at rest and at a given level of exercise by dilating peripheral arterioles.Electrical activity through the AV node depends, to a significant degree, upon calcium influx through the slow channel. By decreasing the influx of calcium, ISOPTIN prolongs the effective refractory period within the AV node and slows AV conduction in a rate related manner.
Normal sinus rhythm is usually not affected, but in patients with sick sinus syndrome, ISOPTIN may interfere with sinus node impulse generation and may induce sinus arrest or sinoatrial block.
Atrioventricular block can occur in patients without preexisting conduction defects (see WARNINGS).
ISOPTIN does not alter the normal atrial action potential or intraventricular conduction time, but depresses amplitude, velocity of depolarization and conduction in depressed atrial fibers. ISOPTIN may shorten the antegrade effective refractory period of accessory bypass tracts. Acceleration of ventricular rate and/or ventricular fibrillation has been reported in patients with atrial flutter or atrial fibrillation and a coexisting accessory AV pathway following administration of verapamil (see WARNINGS).
ISOPTIN has a local anesthetic action that is 1.6 times that of procaine on an equimolar basis.
It is not known whether this action is important at the doses used in man.
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