![]() The bioavailability of nifedipine from nifedipine extended-release tablets relative to immediate release tablets is in the range of 84%-89%. Nifedipine is completely absorbed after oral administration. The reduction in calcium influx by nifedipine causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure. Stores of intracellular calcium in vascular smooth muscle are limited and thus dependent upon the influx of extracellular calcium for contraction to occur. The binding of nifedipine to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. Nifedipine is a peripheral arterial vasodilator which acts directly on vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium. The increased peripheral vascular resistance, an underlying cause of hypertension, results from an increase in active tension in the vascular smooth muscle. The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilatation and, consequently, a reduction in peripheral vascular resistance. ![]() Inert ingredients in the 90mg nifedipine extended-release tablet formulation are: lactose monohydrate, microcrystalline cellulose, hypromellose, magnesium stearate, polyvinyl alcohol, iron oxide red, talc, macrogol/polyethylene glycol 3350, iron oxide yellow, titanium dioxide, lecithin (soy) and iron oxide black. Inert ingredients in the 60mg nifedipine extended-release tablet formulation are lactose monohydrate, microcrystalline cellulose, hypromellose, magnesium stearate, polyvinyl alcohol, titanium dioxide, talc, macrogol/polyethylene glycol 3350, lecithin (soy), iron oxide red, iron oxide black and iron oxide yellow. Inert ingredients in the 30mg nifedipine extended-release tablet formulation are lactose monohydrate, microcrystalline cellulose, hypromellose, magnesium stearate, polyvinyl alcohol, talc, titanium dioxide, macrogol/polyethylene glycol 3350, lecithin (soy), iron oxide yellow and iron oxide black. Nifedipine extended release tablets contain either: 30, 60, or 90 mg of nifedipine for once-a-day oral administration. ![]() The latter compound probably displays other mechanisms (reduced colonic transit, increased water absorption) also responsible for this side effect.Nifedipine is a yellow crystalline substance, practically insoluble in water but soluble in ethanol. We conclude that constipation as a result of some calcium channel blockers may be caused by inhibition of colonic motor activity by nifedipine and, to a lesser extent, by verapamil. This response was also significantly reduced in those taking verapamil compared with the placebo group, although to a much lesser extent than in those taking nifedipine. Each study was preceded by placebo, nifedipine (20 mg), or verapamil (120 mg).Īnalysis of the tracings revealed that nifedipine strongly inhibited the sigmoid myoelectric response to the meal. ![]() Myoelectric sigmoid activity was recorded by means of two clip electrodes introduced within the viscus without preparation for 30 minutes basally and 90 minutes postprandially. Nine healthy male volunteers with no previous abdominal surgery were recruited for the study and underwent three paired studies at two-week intervals. The purpose of the present study was to assess the effects of nifedipine and verapamil on the sigmoid myoelectric response to eating, a physiologic test of colonic motor function. However, the underlying mechanisms for constipation caused by such compounds are not known. This effect may reduce patients' compliance and yield potentially serious consequences. Constipation is not an infrequent side effect complained of by patients taking calcium channel blockers.
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