Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new nifedipine research articles will be listed here shortly after becoming available to us.
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Medical research on nifedipine
Am J Hypertens. 2008 Jul 3;
Hermida RC, Ayala DE, Mojón A, Fernández JR
BackgroundPrevious studies have shown that the circadian pattern of blood pressure (BP) remains unchanged after either morning or evening dosing of several calcium-channel blockers (CCBs), including amlodipine, isradipine, verapamil, nitrendipine, and cilnidipine. This trial investigated the administration-time dependent antihypertensive efficacy of the slow-release, once-a-day nifedipine gastrointestinal-therapeutic-system (GITS) formulation.MethodsWe studied 180 untreated hypertensives (86 men and 94 women), 52.5 +/- 10.7 years of age, randomly assigned to receive nifedipine (30 mg/day) as a monotherapy either upon awakening or at bedtime. BP was measured for 48 h before and after 8 weeks of treatment.ResultsThe BP reduction after treatment was significantly larger with bedtime dosing mainly during night time sleep (P < 0.012). The number of patients with controlled ambulatory BP after treatment was greater with bedtime than morning treatment (P = 0.016). The baseline prevalence of nondipping was unaltered after ingestion of nifedipine on awakening, but reduced from 51 to 35% after bedtime dosing (P = 0.025). The morning surge of BP, a risk factor for stroke, was significantly reduced (P < 0.001) only after bedtime administration of nifedipine. Bedtime in comparison to awakening-time ingestion of nifedipine was also associated with a reduction in the incidence of edema from 13 to 1% (P < 0.001).ConclusionsThe increased efficacy on ambulatory BP as well as the significantly reduced prevalence of edema after bedtime as compared to morning ingestion of nifedipine should be taken into account when prescribing this medication to patients with essential hypertension.American Journal of Hypertension (2008). doi 10.1038/ajh.2008.216American Journal of Hypertension (2008). doi 10.1038/ajh.2008.216.
Physiol Res. 2008; 57(3): 495-8
Zicha J, Dobesová Z, Kunes J
Spontaneously hypertensive rats (SHR) are characterized by enhanced nifedipine-sensitive component of sympathetic vasoconstriction. Our study tried to elucidate the mechanisms responsible for long-term reduction of blood pressure (BP) in SHR subjected to early transient captopril treatment. Adult untreated SHR aged 30-34 weeks were compared with animals subjected to chronic captopril treatment for 6 weeks either in youth (between 4 and 10 weeks of age) or in adulthood (between 24 and 30 weeks of age). Antihypertensive effects of captopril were more pronounced in young than adult SHR. This was due to greater attenuation of sympathetic and nifedipine-sensitive BP components and prevention of residual BP rise in young captopril-treated SHR in which the reductions of nifedipine-sensitive BP component and residual BP persisted for 20 weeks after captopril withdrawal. The magnitude of nifedipine-sensitive component of sympathetic vasoconstriction is decisive for BP maintenance not only in untreated SHR but also in SHR during active captopril treatment by or after its withdrawal.
Obstet Gynecol. 2008 Jul; 112(1): 42-7
Fox NS, Gelber SE, Kalish RB, Chasen ST
OBJECTIVE: To estimate maternal-fetal medicine specialists' practice patterns and perceived risks and benefits to tocolysis. METHODS: We performed a mail-based survey of all Society for Maternal-Fetal Medicine (SMFM) members in the United States. Subjects were asked whether they would recommend tocolysis and what would be their first-line tocolytic in five scenarios: 1) acute preterm labor; 2) maintenance tocolysis after arrested preterm labor; 3) repeat acute preterm labor; 4) preterm premature rupture of membranes (PROM) without contractions; and 5) preterm PROM with contractions. RESULTS: A total of 827 (46%) SMFM members responded. Ninety-six percent, 56%, 56%, 32%, and 29% would recommend tocolysis for acute preterm labor, repeat acute preterm labor, preterm PROM with contractions, preterm PROM without contractions, and maintenance tocolysis, respectively. The most common first-line tocolytic was magnesium for acute preterm labor (45%) and repeat acute preterm labor (41%); nifedipine was the most common maintenance tocolysis (79%). Eighty percent believed tocolysis was associated with moderate or significant benefit in the setting of acute preterm labor; however, fewer than 50% responded similarly for the other four scenarios. In all five scenarios, more than 50% of respondents indicated there was minimal or no risk associated with tocolysis. Having a nonacademic practice was independently associated with the recommendation for tocolysis. CONCLUSION: Almost all maternal-fetal medicine specialists recommend tocolysis in the setting of acute preterm labor, and many recommend tocolysis for other indications. Magnesium and nifedipine are the most commonly prescribed first-line tocolytics. LEVEL OF EVIDENCE: III.
Neuroscience. 2008 Jun 5;
Wang JH, Wang F, Yang MJ, Yu DF, Wu WN, Liu J, Ma LQ, Cai F, Chen JG
The fat-derived hormone leptin regulates food intake and body weight in part by modulating the activity of neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (ARC). To investigate the electrophysiological activity of these neurons and their responses to leptin, we recorded whole-cell calcium currents on NPY and POMC neurons, which we identified by morphologic features and immunocytochemical identification at the end of recording. Leptin decreased the peak amplitude of high voltage-activated calcium currents (I(HVA)) in the isolated neurons from ARC, which were subsequently shown to be immunoreactive for NPY. The inhibition was prevented by pretreatment with inhibitors of Janus kinase 2 (JAK2) and mitogen-activated protein kinases (MAPK). In contrast, leptin increased the amplitude of I(HVA) in POMC-containing neurons. The stimulations of I(HVA) were inhibited by blockers of JAK2 and phosphatidylino 3-kinase (PI3-k). Both of these effects were counteracted by the L-type calcium channel antagonist nifedipine, suggesting that L-type calcium channels were involved in the regulation induced by leptin. These data indicated that leptin exerted opposite effects on these two classes of neurons. Leptin directly inhibited I(HVA) in NPY neurons via leptin receptor (LEPR) -JAK2-MAPK pathways, whereas evoked I(HVA) in POMC neurons by LEPR-JAK2-PI3-k pathways. These neural pathways and intracellular signaling mechanisms may play key roles in regulating NPY and POMC neuron activity, anorectic action of leptin and, thereby, feeding.
Liver Transpl. 2008 Jun 25; 14(7): 1020-1028
Galioto A, Semplicini A, Zanus G, Fasolato S, Sticca A, Boccagni P, Frigo AC, Cillo U, Gatta A, Angeli P
The aim of this study was to compare nifedipine and carvedilol in the treatment of de novo arterial hypertension after orthotopic liver transplantation (OLT). The study included 50 patients who developed arterial hypertension after OLT. Twenty-five patients received nifedipine (group A), and 25 received carvedilol (group B). Patients were defined as intolerant to nifedipine or carvedilol if severe adverse effects developed. These patients stopped the first drug and were switched to the other one. Patients were defined as full responders to monotherapy if there was normalization of blood pressure, and they were defined as partial responders by the need to add a second antihypertensive drug, ramipril. The 2 groups of patients were similar for baseline conditions. At the end of the study, patients intolerant to monotherapy were 48% of group A and 12.5% of group B (P < 0.01). Full responders were 20% of group A and 33.33% of group B (P < 0.01). Partial responders were 22% of group A and 54.1% of group B (P < 0.01). The addition of ramipril normalized blood pressure in 19% of partial responders to monotherapy (75% in partial responders to nifedipine and 30% in partial responders to carvedilol, P < 0.01). In responders to either monotherapy or combined therapy, there was a significant improvement of renal function. In responders to carvedilol, but not in responders to nifedipine, the daily dose of tacrolimus at 1 year should be reduced to 50% compared to the baseline dose to maintain the blood trough level in the therapeutic range. Liver Transpl 14:1020-1028, 2008. (c) 2008 AASLD.
[The use of nifedipine as a corrector of extrapyramidal side-effects of classical neuroleptics.]
Zh Nevrol Psikhiatr Im S S Korsakova. 2008; 108(6): 28-33
Popov MI
The aim of the article was to study efficacy and safety of nifedipine in the correction of extrapyramidal side-effects emerged during conventional neuroleptics therapy. Fifty-one patients diagnosed with paranoid schizophrenia received haloperidol in combination with nifedipine (25 patients) or haloperidol only (26 patients) during 26 weeks. Dynamics of psychopathological symptoms and extrapyramidal disorders were measured with PANSS, CGI, BARS, SARS and AIMS. Patients receiving haloperidol in combination with nifedipine had the lower AIMS scores indicating appearances of dyskinesia and less marked (on the trend to statistical significance) SARS scores measuring parkinsonian symptoms as compared to patients receiving monotherapy with haloperidol. The administration of nifedipine in combination with haloperidol did not reduce the therapeutic efficacy of the latter and did not lead to the increase of side-effects. The data obtained suggest that nifedipine may be used as a perspective corrector of extrapyramidal disorders caused by classical neuroleptics.
Polim Med. 2007; 37(4): 21-38
Zgoda MM, Nachajski MJ, Kołodziejczyk MK, Woskowicz MH, Lukosek M
Research was conducted into the properties and identity of the products of oxyethylation of cholic acid, which were obtained with the use of a selective catalyst (K4). The 1HNMR method was employed to assess the content of oxyethylated segments and the analytic level of hydrophilic-lipophilic balance (HLB). Surface activity of the products of oxyethylation in water and 0.1 M HCL was examined and cmc and gamma(25)cmc were determined. These were employed to calculate the thermodynamic potential for micelle formation deltaG(o)m and the surface occupied by the lipophilic structure of the surfactant at the phase boundary. Basic viscosity and hydrodynamic values were determined for the solubilizers and their micellar adducts with diclofenac, ketoprofen, fenofibrate, gemfibrozil and nifedipine. In addition, the amount of solubilized therapeutic agents c/s/ was examined by means of the spectroscopic method and the H/L balance in a solid state. The results obtained in the course of research served as a basis for determining the solubilization mechanism and the stability of the micellar adduct for the purpose of application.
J Membr Biol. 2008 Apr; 222(3): 151-66
Yamada M, Ohta K, Niwa A, Tsujino N, Nakada T, Hirose M
Early afterdepolizations (EADs) induced by suppression of cardiac delayed rectifier I (Kr) and/or I (Ks) channels cause fatal ventricular tachyarrhythmias. In guinea pig ventricular myocytes, partial block of one of the channels with complete block of the other reproducibly induced EADs. Complete block of both I (Kr) and I (Ks) channels depolarized the take-off potential and reduced the amplitude of EADs, which in some cases were not clearly separated from the preceding action potentials. A selective L-type Ca(2+) (I (Ca,L)) channel blocker, nifedipine, effectively suppressed EADs at submicromolar concentrations. As examined with the action potential-clamp method, I (Ca,L) channels mediated inward currents with a spike and dome shape during action potentials. I (Ca,L) currents decayed mainly due to inactivation in phase 2 and deactivation in phase 3 repolarization. When EADs were induced by complete block of I (Kr) channels with partial block of I (Ks) channels, repolarization of the action potential prior to EAD take-off failed to increase I (K1) currents and thus failed to completely deactivate I (Ca,L) channels, which reactivated and mediated inward currents during EADs. When both I (Kr) and I (Ks) channels were completely blocked, I (Ca,L) channels were not deactivated and mediated sustained inward currents until the end of EADs. Under this condition, the recovery and reactivation of I (Ca,L) channels were absent before EADs. Therefore, an essential mechanism underlying EADs caused by suppression of the delayed rectifiers is the failure to completely deactivate I (Ca,L) channels.
Clin Exp Pharmacol Physiol. 2008 Jun 18;
El-Gowilly SM, Ghazal AR, Gohar EY, El-Mas MM
1. Nicotine is implicated in smoking-related renovascular impairment and worsening of existing nephropathies. In the present study, we investigated whether nicotine aggravates the deleterious effect of the immunosuppressant drug cyclosporine A (CsA) on renal vasodilation induced by the beta-adrenoceptor agonist isoprenaline. 2. Bolus isoprenaline (0.03-8.0 micromol) elicited dose-dependent vasodilation of phenylephrine-preconstricted perfused kidneys that was attenuated by infusion at 5 mL/min of nicotine (5 x 10(-4) mol/L) or CsA (2 micromol/L). Further, chronic administration of nicotine (0.4 mg/kg per day) or CsA (20 mg/kg per day) for 3 weeks reduced isoprenaline-induced vasodilation and elevated plasma urea and creatinine concentrations, effects that were magnified when both nicotine and CsA were administered concurrently. 3. The role of endothelial and smooth muscle signalling in the acute nicotine/CsA renovascular interaction was investigated. Vasodilation caused by 0.25 micromol isoprenaline was attenuated by 6 micromol/L propranolol and 10 mmol/L tetraethylammonium (TEA), potentiated by 100 micromol/L hexamethonium and 7 micromol/L diclophenac, and virtually abolished in 80 mmol/L KCl-preconstricted tissues. N(G)-Nitro-l-arginine (l-NNA; 200 micromol/L), methylene blue (10 micromol/L), 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane-sulphonate (CHAPS; 0.2% for 30 s), nifedipine (750 nmol/L), atropine (1 micromol/L) and SQ22536 (an adenylyl cyclase inhibitor; 3 x 10(-5) mol/L) had no effect on isoprenaline responses. 4. Nicotine (5 x 10(-4) mol/L) reduced isoprenaline-induced vasodilation and this effect was potentiated by concurrent CsA (2 micromol/L) infusion. Nicotine-induced impairment of the vasodilator response to isoprenaline was reduced by hexamethonium and potentiated by l-NNA, methylene blue, CHAPS and nifedipine. Alternatively, CsA exacerbation of the nicotine-isoprenaline interaction was abolished by propranolol, l-NNA, methylene blue, CHAPS, l-arginine, TEA and nifedipine. 5. In summary, nicotine and CsA produce additive impairment of kidney function and beta-adrenoceptor-mediated renovascular control, nitric oxide (NO)-cGMP signalling tonically restrains nicotine-induced impairment of isoprenaline vasodilation and the endothelial NO-K(+) pathway modulates the aggravating effect of CsA on nicotine-isoprenaline interactions.
Effects of Arecoline on Testosterone Release in Rats.
Am J Physiol Endocrinol Metab. 2008 Jun 17;
Wang SW, Hwang GS, Chen TJ, Wang PS
ABSTRACT Arecoline is one of the major components of betel nuts, which have been consumed as chewing gum in Southeast Asia. In this study, the effects of arecoline on testosterone (T) secretion were explored. Male rats were injected with human chorionic gonadotropin (hCG, 5 IU/kg) or arecoline (1 microg/kg) plus hCG via a jugular catheter. Blood samples were collected at several time intervals subsequent to the challenge. Rat anterior pituitary was treated with gonadotropin releasing hormone in vitro with or without arecoline and then the concentrations of luteinizing hormone (LH) in the medium were measured. Rat Leydig cells were purified by Percoll density gradient centrifugation and incubated with arecoline, hCG, forskolin, 8-Br-cAMP, nifedipine, nimodipine, or tetrandrine at 34 degrees C for 1 h. A single intravenous injection of arecoline resulted in an increase of hCG-induced level of plasma T. Administration of arecoline (10(-8)-10(-6) M) in vitro increased T production in Leydig cells. The stimulatory effect of arecoline on T release in vitro was enhanced by hCG (0.001 IU/ml), forskolin (10(-6) M) or 8-Br-cAMP (10(-5) M). By contrast, nifedipine, nimodipine or tetrandrine inhibited the increased T concentrations induced by arecoline. By the Western blot, it showed that arecoline increases steroidogenic acute regulatory (StAR) protein expression compared to vehicle. These results suggested that arecoline stimulates testosterone production by acting directly on Leydig cells via mechanisms involving an activation of L-type calcium channels, increasing the activity of 17beta-hydroxysteroid dehydrogenase and enhancing the expression of StAR. Key words: arecoline, , Leydig cell, , L-type calcium channel, , testosterone.