Pharmacokinetics and pharmacodynamics of conventional and slow release forms of nifedipine in essential hypertensive patients.

Abstract

In patients with essential hypertension, the pharmacokinetics of nifedipine in 2 forms (capsule, 10 mg nifedipine dissolved in an organic solvent ; slow release tablet, 20 mg nifedipine) and their pharmacodynamic effectiveness on arterial pressure were studied. The maximum plasma concentration was higher and achieved more rapidly after application of the capsule than after the retard tablet (p <0.01). The plasma half-time of nifedipine in the capsule was shorter than that in the retard tablet (p <0.05). The absorption rate of nifedipine from the capsule tended to be larger than that from the retard tablet. Plasma concentrations of nifedipine, measured 12 hr after the dosing of the retard tablet during chronic treatment, were not different from those after the acute administration of the retard tablet, suggesting that no accumulation of nifedipine occurs. The capsule of nifedipine elicited prompt and profound hypotension with short duration, while the retard tablet produced a hypotensive effect with relatively slow onset and long duration. Arterial pressure reduction was maintained throughout the day using 12 hourly dose of the retard tablet. During the chronic treatment the maximum hypotensive effect was observed 4 weeks after the start of treatment. Twelve hourly administration of the retard tablet is a convenient regimen for the long-term control of mild to severe essential hypertension.nifedipine ; slow release form ; conventional form ; antihypertensive therapy ; essential hypertension Nifedipine is a potent vasodilator, which relaxes vascular smooth muscle probably by its inhibitory effect on the transmembrane influx of calcium (Fleckenstein et al. 1972 ). It has been demonstrated that this drug exerts a prompt and marked hypotensive effect when administered to hypertensive patients (Murakami et al, 1972;Aoki et al, 1976;Guazzi et al. 1977;Pedersen and Mikkelsen 1978;Imai et al. 1980) and the drug has been accepted as a critical therapeutic for several forms of hypertension (Guazzi et al. 1983;Massie et al. 1984; Muhller et

Oral nifedipine as a premedication for induced hypotension in functional endoscopic sinus surgery (FESS)

“…We examined the use of nifedipine 10 mg in 3 pilot cases before starting in the study, but we noticed minimal reduction in MAP, and then we decided to examine nifedipine 20 mg. The result of our study showed that oral nifedipine (20 mg) one hour before induction of anesthesia markedly reduces the amount of GTN required to decrease MAP during FESS by 80% used in control group (3.3 ± 3.4 mg in nifedipine versus 16 ± 6.4 mg in control) These findings confirm a previous study by Ahmad1 et al they investigated the pharmacokinetic of nifedipine in healthy adult male human volunteers which showed that use of oral nifedipine reduced MAP [18], is also in agreement with our study, and Imai et al examined the effect of nifedipine in essential hypertensive patients, when the conventional form of nifedipine (soft capsule containing 10 mg of dissolved nifedipine) was administered orally, there was a rapid hypotensive effect occurring maximally at 1 h after administration and disappearing within 7 h [9]. The probable mechanism of reducing blood pressure by promote vasodilator activity (and reduce blood pressure) by reducing calcium influx into vascular smooth muscle cells by interfering with voltageoperated calcium channels (and to a lesser extent receptoroperated channels) in the cell membrane [23].…”

“…Nifedipine is a potent vasodilator, which relaxes vascular smooth muscle probably by its inhibitory effect on the transmembrane influx of calcium, and it is very effective in the treatment of severe hypertension and hypertensive emergency. When the conventional form of nifedipine (soft capsule containing 10 mg of dissolved nifedipine) was administered orally, there was a rapid hypotensive effect occurring maximally at 1 h after administration and disappearing within 7 h [9]. The rationale behind using oral nifedipine as an agent for inducing hypotension in our study is to induce gradual smooth hypotension without rapid swing in BP by IV hypotensive agents The current study was designed to evaluate the effect of oral nifedipine on the hemodynamic changes, the quality of the operative field, blood loss and the amount of nitroglycerine used in patients undergoing FESS under general anesthesia.…”

Nicardia® XL (Nifedipine Extended Release): Technologically Advanced GITS Formulation Ensures Robust Efficacy and Assured Safety

“…The hypotensive effect of the conventional form of Nifedipine is observed maximally at 1 hour after administration and disappears within 7 hours. As a result, Nifedipine has been shown to exert a prompt and marked hypotensive effect when administered to hypertensive patients 14 . Rapid and profound vasodilation by short-acting Nifedipine has been associated with reflex sympathetic nervous system (SNS) activation leading to flushing, tachycardia, worsening myocardial ischemia, and cerebrovascular ischemia 14 .…”

“…As a result, Nifedipine has been shown to exert a prompt and marked hypotensive effect when administered to hypertensive patients 14 . Rapid and profound vasodilation by short-acting Nifedipine has been associated with reflex sympathetic nervous system (SNS) activation leading to flushing, tachycardia, worsening myocardial ischemia, and cerebrovascular ischemia 14 . It has been suggested that a higher incidence of cardiovascular events associated with Nifedipine may be due to reflex activation of the SNS 20 .…”

Glycosuria medicated with ipragliflozin and nifedipine or ipragliflozin and candesartan: a case report

“…Approximately 3.5 hours after breakfast random urine and blood samples were collected as indicated in the schedule shown in Figure 1 . According to the drug pharmacokinetics data, nifedipine is rapidly absorbed, reaching maximum plasma concentration within 3 hours and returns to basal level within 24 hours [ 4 ]. Therefore, we collected urine samples at days 3, 4, and 5 and a blood sample at day 5 of nifedipine treatment.…”