Effects of cyclosporin, nifedipine and phenytoin on gingival myofibroblast transdifferentiation in monkeys

Abstract Objective: Myofibroblasts have been associated with the development of several pathologic fibrotic conditions. This longitudinal study aims to assess the proliferative and antiapoptotic effects of cyclosporin, nifedipine and phenytoin on gingival connective tissue cells of nonhuman primate, as well as to analyze a possible role of myofibroblasts in gingival overgrowth. Materials and Methods: Gingival samples from the right superior canine area were obtained from 12 male monkeys ( Sapajus spp ) to comprise the control group. After one week, the animals were randomly assigned to three groups, which received daily oral doses of cyclosporin, nifedipine or phenytoin for 120 days. Gingival samples were collected from the left superior canine area of two animals of each group at 52 and 120 days. Histological sections were stained with hematoxylin and eosin, and immunoreacted against α-SMA, Ki- 67 and bcl-2. Results: α-SMA immunoreaction was negative in the control and experimental groups. Similarly, no difference between groups concerning immunostaining against Ki-67 and bcl-2 was observed in connective tissue cells. Conclusion: Based on this methodology, it may be concluded that gingival overgrowths induced by cyclosporin, nifedipine and phenytoin are not associated with neither myofibroblast transdifferentiation, proliferation nor apoptosis of gingival connective cells in monkeys.

To compare the effectiveness of nifedipine and glyceryl trjnjtrate patch jn prevention of preterm Labour

Objective: To assess the effectiveness of Nifedipine and Glyceryl trinitrate patch in prolonging the pregnancy for more than 48 hours

Methodology: This was a randomized control study. Fifty patients with preterm labour meeting the inclusion criteria were inducted in study and randomly allocated to the treatment group A [Nifedipine] and group B [Glyceryl trinitrate patch, GTN]. After taking consent from the patients, all the details were documented on a proforma and tocolysis was started with either of these tocolytics according to a preset protocol

Results: Nifedipine was found to be more effective than GTN, as prolongation of pregnancy beyond 48 hours was more frequent [74%] with nifedipine than GTN [40%] with P value <0.05 . Similarly prolongation beyond 7 days was also more frequent [32%] with nifedipine as compared with GTN [24%]. Most common adverse effect found with nifedipine was headache followed by palpitations and hypotension. GTN patch had a better side effect profile with most of the patients being asymptomatic. Fetal distress was noticed more in GTN group as compared with nifedipine

Conclusion: Nifedipine, as a tocolytic, is found to be more effective in pregnancy prolongation when compared with Glyceryl trinitrate but has frequent maternal adverse drug effects. Glyceryl trinitrate patch is well tolerated by the patients with preterm labour with relatively fewer side effects

Antischistosomal activity of a calcium channel antagonist on schistosomula and adult Schistosoma mansoni worms

Current schistosomiasis control strategies are largely based on chemotherapeutic agents and a limited number of drugs are available today. Praziquantel (PZQ) is the only drug currently used in schistosomiasis control programs. Unfortunately, this drug shows poor efficacy in patients during the earliest infection phases. The effects of PZQ appear to operate on the voltage-operated Ca2+channels, which are located on the external Schistosoma mansoni membrane. Because some Ca2+channels have dihydropyridine drug class (a class that includes nifedipine) sensitivity, an in vitro analysis using a calcium channel antagonist (clinically used for cardiovascular hypertension) was performed to determine the antischistosomal effects of nifedipine on schistosomula and adult worm cultures. Nifedipine demonstrated antischistosomal activity against schistosomula and significantly reduced viability at all of the concentrations used alone or in combination with PZQ. In contrast, PZQ did not show significant efficacy when used alone. Adult worms were also affected by nifedipine after a 24 h incubation and exhibited impaired motility, several lesions on the tegument and intense contractility. These data support the idea of Ca2+channels subunits as drug targets and favour alternative therapeutic schemes when drug resistance has been reported. In this paper, strong arguments encouraging drug research are presented, with a focus on exploring schistosomal Ca2+channels.

Serotonin contracts the rat mesenteric artery by inhibiting 4-aminopyridine-sensitive Kv channels via the 5-HT2A receptor and Src tyrosine kinase

Serotonin (5-hydroxytryptamine (5-HT)) is a neurotransmitter that regulates a variety of functions in the nervous, gastrointestinal and cardiovascular systems. Despite such importance, 5-HT signaling pathways are not entirely clear. We demonstrated previously that 4-aminopyridine (4-AP)-sensitive voltage-gated K+ (Kv) channels determine the resting membrane potential of arterial smooth muscle cells and that the Kv channels are inhibited by 5-HT, which depolarizes the membranes. Therefore, we hypothesized that 5-HT contracts arteries by inhibiting Kv channels. Here we studied 5-HT signaling and the detailed role of Kv currents in rat mesenteric arteries using patch-clamp and isometric tension measurements. Our data showed that inhibiting 4-AP-sensitive Kv channels contracted arterial rings, whereas inhibiting Ca2+-activated K+, inward rectifier K+ and ATP-sensitive K+ channels had little effect on arterial contraction, indicating a central role of Kv channels in the regulation of resting arterial tone. 5-HT-induced arterial contraction decreased significantly in the presence of high KCl or the voltage-gated Ca2+ channel (VGCC) inhibitor nifedipine, indicating that membrane depolarization and the consequent activation of VGCCs mediate the 5-HT-induced vasoconstriction. The effects of 5-HT on Kv currents and arterial contraction were markedly prevented by the 5-HT2A receptor antagonists ketanserin and spiperone. Consistently, alpha-methyl 5-HT, a 5-HT2 receptor agonist, mimicked the 5-HT action on Kv channels. Pretreatment with a Src tyrosine kinase inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine, prevented both the 5-HT-mediated vasoconstriction and Kv current inhibition. Our data suggest that 4-AP-sensitive Kv channels are the primary regulator of the resting tone in rat mesenteric arteries. 5-HT constricts the arteries by inhibiting Kv channels via the 5-HT2A receptor and Src tyrosine kinase pathway.

Targeting CYP450 modulation to decrease the risk of induced cataract in the experimental model.

Background: Diabetes is one of the major causes of cataract. Some drugs prescribed for the treatment of diabetes are the modulators of CYP450, which may alter the risk of cataract. Objective: To study the effect of CYP450 modulation in galactosemic cataract. Materials and Methods: Male Sprague-Dawley suckling rats were allotted to four groups (n = 6), as follows: Group 1: Normal control, Group 2: Galactose control, Group 3: CYP450 inhibitor pretreated and Group 4: CYP450 inducer pretreated. Cataract was induced in animals of all groups except group 1 by feeding them galactose (50%), 21 days after parturition. From the eighteenth day of life, CYP450 inhibitor (nifedipine; 8.1 mg/kg) and CYP450 inducer (pioglitazone; 3.8 mg/kg) were given orally to groups 3 and 4, respectively. The maturation pattern of the cataract was observed by an operating microscope, every third day. Biochemical changes in the lenses of all groups, for example, CYP450 activity expressed as µM NADPH oxidized / unit time, alterations in the levels of total proteins, soluble proteins, and reduced glutathione (GSH) following the induction of cataract, were estimated. Results: The microscopic examination of the lenses indicated that CYP450 inhibitor pre-treatment delayed (fourteenth day) the occurrence of cataract, while CYP450 inducer pretreatment demonstrated an early (ninth day) cataract as compared to galactose control rats (twelfth day). A significant decrease and increase in CYP450 activity was observed with the CYP450 inhibitor and inducer pre-treatment, respectively. There was no alteration in the GSH level, but a significant increase in total and soluble protein was found in groups 3 and 4 as compared to group 2. Conclusion: CYP450 may have a role in the initiation of cataract without any effect on the maturation pattern, as revealed by the delayed occurrence of cataract with the CYP450 inhibitor and an early onset of cataract with the CYP450 inducer.

[Comparative study of effects of fast release sublingual versus chewing-swallowing nifedipine on blood pressure decline in hypertension emergencies]

Hypertensive emergency is one of the most important conditions in the emergency department with high mortality and morbidity if not treated effectively. Hypertensive emergency is commonly treated with sublingual nifedipine. This drug is very short acting and it may decrease blood pressure suddenly, resulting in dangerous side effects such as myocardial ischemia and sudden cardiac death. We intended to find of a safer route of administration. Therefore, we compared the rate of blood pressure decline following sublingual and chewing-swallowing routes of administration. A quasi-experimental clinical study was performed on 160 patients with hypertensive emergency. All patients with blood pressure >/= 210/125 mmHg and without sign of end organ damage were selected randomly into those receiving sublingual or chewing-swallowing 10 mg nifedipine capsules. The data collection tools consisted of an information sheet and a semi-automatic sphygmomanometer. Information sheet had two parts, the first was related to demographic data and the second part was the check list of blood pressure [systolic, diastolic, mean] and heart rate at 5, 10, 20, 30, 60 and 120 minutes after administration. All data include quantitative and qualitative were analyzed with paired comparison, t-test and Chi-square. The results of this study showed that there was significantly greater fall in the rate of blood pressure in the sublingually-treated group compared with chewing-swallowing group at 5, 10 and 20 minutes after taking 10 mg nifedipine [P = 0.04, 0.01, 0.06 respectively]. There was no significant difference in diastolic blood pressure between both groups during the time of study. After 30 minutes the fall in systolic and diastolic blood pressures in both groups was similar. There was no significant difference in heart rate among both groups but there is some trend to the increase the rate. There was 23% decrease in mean basic blood pressure among the patients before and after treatment in sublingual and chewing-swallowing groups [P=0.0001]. There was no significant correlation of blood pressure abatement rate in both groups as dependent variables of age, sex, positive history of risk factors and current drugs as independent variable. The chewing-swallowing route may be safer than sublingual route since it reduces pressure less rapidly during the first 20 minutes of administration

Efeitos hemodinâmicos da nifedipina na inibição do trabalho de parto prematuro / Hemodynamics effects of nifedipine as a tocolytic agent in preterm labour

Realizou-se revisão da literatura a respeito do uso da nifedipina no trabalho de parto prematuro, descrevendo-se os principais aspectos farmacológicos, eficiência como agente de tocólise, bem como os potenciais efeitos adversos maternos e fetais, com ênfase na hemodinâmica útero-placentária. De acordo com as evidências atuais, a nifedipina é a medicação de escolha para tocólise, apresentando boa eficácia na inibição das contrações uterinas, custo mais baixo quando comparada aos demais fármacos e melhor tolerância materna por ter menos efeitos colaterais, sobretudo em relação aos betamiméticos. Os efeitos colaterais maternos mais freqüentes com o uso da medicação são a cefaléia, a fadiga e o rubor cutâneo. Os efeitos adversos fetais são pouco conhecidos. Pesquisas futuras são necessárias objetivando encontrar um regime posológico padrão que apresente boa eficácia tocolítica e nenhum ou mínimos efeitos adversos para o binômia materno-fetal.

A literature review on nifedipine in preterm labour was performed describing its pharmacological aspects, efficiency as tocolytic agent and its potential maternal-fetal side effects, emphasizing utero-placental hemodynamics. Recent evidence supports the use of nifedipine as medication of choice for tocolysis, presenting a satisfactory action to inhibit uterine contraction, lower proce when compared to other tocolytics agents and better maternal tolerance. The most frequent side effects with nifedipine for tocolysis are cutaneous flush, headache and fatigue. Fetal side effects are less known. Future research is necessary to find an ideal nifedipine posologic scheme which presents a satisfactory tocolysis performance and none or minimal maternal-fetal side effects.

Ptychodiscus brevis toxin decreases the spontaneous activity of rat right atria involving muscarinic receptors and potassium channels.

Marine dinoflagellate Ptychodiscus brevis toxin (PbTx), is known to produce toxic effects on cardiovascular system. The present experiments were conducted to evaluate the effect of synthetic phosphorus containing Ptychodiscus brevis toxin on spontaneously beating right atrium in vitro. The PbTx (0.84-84 microM) decreased the rate and force of right atrial contractions in a concentration-dependent manner. Ethanol, a vehicle present in highest concentration of PbTx, had no effect on atrial rate or force of contraction. Pretreatment with atropine blocked the PbTx-induced decrease in atrial rate and force of contraction. The tetraethylammonium, a potassium channel blocker, blocked the PbTx-induced decrease in atrial rate and force, where as, L-type of calcium channel blocker, nifedipine blocked the PbTx-induced force of contraction but not the rate changes. The results indicate that the PbTx decreased the atrial rate and force of contraction via cholinergic receptors involving K+ channel.

High susceptibility of activated lymphocytes to oxidative stress-induced cell death

The present study provides evidence that activated spleen lymphocytes from Walker 256 tumor bearing rats are more susceptible than controls to tert-butyl hydroperoxide (t-BOOH)-induced necrotic cell death in vitro. The iron chelator and antioxidant deferoxamine, the intracellular Ca2+ chelator BAPTA, the L-type Ca2+ channel antagonist nifedipine or the mitochondrial permeability transition inhibitor cyclosporin A, but not the calcineurin inhibitor FK-506, render control and activated lymphocytes equally resistant to the toxic effects of t-BOOH. Incubation of activated lymphocytes in the presence of t-BOOH resulted in a cyclosporin A-sensitive decrease in mitochondrial membrane potential. These results indicate that the higher cytosolic Ca2+ level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving the participation of mitochondrial permeability transition.

O presente estudo demonstra que linfócitos ativados de baço de ratos portadores do tumor de Walker 256 são mais susceptíveis à morte celular necrótica induzida por tert-butil hidroperóxido (t-BOOH) in vitro quando comparados aos controles. O quelante de ferro e antioxidante deferoxamina, o quelante intracelular de Ca2+ BAPTA, o antagonista de canal de Ca2+ nifedipina ou o inibidor da transição de permeabilidade mitocondrial ciclosporina-A, mas não o inibidor de calcineurina FK-506, inibiram de maneira similar a morte celular induzida por t-BOOH em linfócitos ativados e controles. Os linfócitos ativados apresentaram redução do potencial de membrana mitocondrial induzida por t-BOOH num mecanismo sensível a ciclosporina-A. Nossos resultados indicam que o aumento da concentração de Ca2+ citosólico em linfócitos ativados aumenta a susceptibilidade dos mesmos à morte celular induzida por estresse oxidativo, num mecanismo envolvendo a participação do poro de transição de permeabilidade mitocondrial.

Role of ion channel modifiers in reversal of morphine-induced gastrointestinal inertia by prokinetic agents in mice.

Prokinetic drugs like mosapride, domperidone etc, are used to treat gastrointestinal delay. Though the receptor-mediated actions of these agents have been studied, involvement of ion channels in reversing morphine-induced gastrointestinal inertia by prokinetic agents has not been explored. Charcoal meal test was used to measure small intestinal transit (SIT) in adult male Swiss albino mice. Animals were given ion channel modifiers and prokinetic drugs intragastrically. Reversal of morphine-induced gastrointestinal delay by mosapride was decreased significantly by CaCl2, minoxidil and glibenclamide. Similarly, domperidone's effect on morphine was decreased by CaCl2, nifedipine, minoxidil and glibenclamide significantly. The results reveal that ion channel modifiers counteract the prokinetic effects of mosapride or domperidone.

[Highlighting the expression of a nifedipine resistant l type calcium current in human atrial cardiomyocytes]

In the heart, two types of calcium currents were described, the L-and T-type. In addition to these two types, a dihydropyridine-resistant Ca[2+] component has been described to be up-regulated in rat ventricular cardiomyocytes during their differentiation-dedifferentiation process. The aim of our study is to examine if such calcium current component is present in human cardiomyocytes. The patch clamp technique was used to record Ca[2+] current in atrial cells. In the presence of 2 micro M nifedipine, residual current was activated [-2.7 +/- 0.7 pA/pF, n=6] in the same voltage range as the L-type, nifedipine-sensitive Ca[2+] current [-2.1 +/- 0.4 pA/pF, n=6], but its steady-state inactivation was negatively shifted by 10 mV. This nifedipine-resistant Ca[2+] current was completely blocked by 500 micro M cadmium chloride and significantly enhanced by 1 micro M isoproterenol [-7.5 +/- 0.5 pA/pF, n=6; p <0.01]. These results give evidence that a nifedipine-resistant Ca[2+] current, similar to the one which has been shown to be developmentally expressed in rat ventricular cardiomyocytes, is observed in human atrial cells. Its molecular identity, its expression level as well as its role in pathophysiologic conditions remain to be studied

effect of treatment with nifedipine on malondiaklehyde contents, and reduced glutathione levels in serum of pre-eclamptic women

Increased lipid peroxidation and reduced anti-oxidant activity may contribute to the development of complications in pregnancy. The objective of this study was to test the hypothesis that maternal serum lipid peroxidation products are increased and anti-oxidant decreased in women with mild and moderate pre-eclampsia; and study the effect of treatment with nifedipine on the above parameters. Malondialdehyde [MDA], and reduced glutathione [GSH] were measured in maternal serum in the 3rd trimester of pregnancy, in normotensive pregnant women [n=15], mild pre-eclamptic untreated control [n=6], moderate pre-eclamptic untreated control [n=6], mild and moderate pre-eclamptic women treated with nifedipine [n=6], and [n=8], respectively. Maternal serum levels of MDA and GSH were higher and lower, respectively in both cases of pre-eclampsia when compared to normotensive pregnant controls. Treatment with nifedipine shows a significant decrease and increase, respectively in MDA contents GSH levels in serum of both cases of pre-eclampsia when compared to normal pregnant. Lipid peroxidation is involved in the pathogenesis of maternal pre-eclampsia, as evidenced by a significant increase in MDA contents and reduction of protective anti-oxidant system manifested by GSH levels. Treatment with nifedipine effectively lowers blood pressure; reduce serum MDA contents and increases serum GSH levels in pre-eclamptic women

Kinetics and mechanisms of cholesterol esterase inhibition by cardiovascular drugs in vitro.

Cardiovascular drugs such as lovastatin, simvastatin, amlodipine besylate, nifedipine, and hydralazine hydrochloride inhibit cholesterol esterase (CEase) in vitro. In the present paper, an attempt was made to determine kinetically the reaction mechanism for CEase inhibition by these drugs. The inhibition constant, Ki, for the mixed-type inhibition of CEase by these drugs in the presence of triton-X-100 or taurochloate were measured. Moreover, the pKi values were correlated with the molecular weights of these drugs. In conclusion, the fact that these drugs lower cholesterol levels in the plasma low-density lipoprotein may be partially due to the CEase inhibition by these drugs.

Hypothyroid state reduces calcium channel function in 18-day pregnant rat uterus.

Hypothyroidism significantly reduced the mean amplitude and increased the mean frequency of spontaneous rhythmic contractions in 18 day pregnant rat uterus. Nifedipine (10(-12)-10(-9) M) and diltiazem (10(-10)-10(-6) M) caused concentration related inhibition of the myogenic responses of the uterine strips obtained from both pregnant and hypothyroid state. However, nifedipine was less potent (IC50:2.11 x 10(-11) M) in pregnant hypothyroid state as compared to pregnant control (IC50: 3.1 x 10(-12) M). Similarly, diltiazem was less potent (IC50: 3.72 x 10(-9) M) in inhibiting the uterine spontaneous contractions in hypothyroid than in pregnant rat uterus (IC50:5.37 x 10(-10) M). A similar decrease in the sensitivity to nifedipine and diltiazem for reversal of K+ (100 mM)-induced tonic contraction and K(+)-stimulated 45Ca2+ influx was observed with these calcium channel antagonists in uterus obtained from hypothyroid pregnant rats compared to the controls. Nifedipine-sensitive influx of 45Ca(2+)-stimulated either by K+ (100 mM) or by Bay K8644 (1,4-dihydro-2,6-methyl-5-nitro-4-[2'-(trifluromethyl)phenyl]-3-pyridine carboxylic acid methyl ester) (10(-9) M) was significantly less in uterine strips from hypothyroid rats compared to controls. The results suggest that the inhibition of uterine rhythmic contractions may be attributable to a reduction in rat myometrial Ca2+ channel function in the hypothyroid state.

Effect of nifedipine and amlodipine on dead space wound healing in rats.

Effect of two calcium channel blockers (CCBs) nifedipine and amlodipine, was studied on normal and steroid depressed wound healing in albino rats, using the dead space wound model. The drugs enhanced normal healing as evidenced by increase in tensile strength of 10 days old granulation tissue. There was neither a significant change in the hydroxyproline level (or collagen) nor a change in the glycosaminoglycan content in granulation tissue. However, lysyloxidase level was increased significantly. The increase in tensile strength could thus be attributed to better cross-linking and maturation of collagen rather than collagen synthesis per se. The drugs were also able to overcome steroid depressed wound healing. It is likely that the prohealing effects may be related to the improved antioxidant status too, since superoxide dismutase levels were observed to be higher in the CCB- treated animals.

Effects of calcium, strontium, and barium on isolated phrenic nerve-diaphragm preparation of rat and their interactions with diltiazem and nifedipine.

Calcium (Ca2+), strontium (Sr2+), and barium (Ba2+) are expected to exert similar chemical and pharmacological effects. The effects of barium, strontium and calcium were studied on the contractions of rat phrenic nerve-diaphragm preparations, following electrical stimulation and their interactions with nifedipine (nif) and diltiazem (DZM) were also studied. Low doses of strontium chloride (SrCl2), barium chloride (BaCl2) and calcium chloride (CaCl2) were able to increase the force of contraction of the rat diaphragm when actively stimulated. Diltiazem inhibited the stimulant effects of Sr2+, Ba2+, and Ca2+. On the other hand, nifedipine blocked the effects of Sr2+ and Ca2+ but potentiated the effects of Ba2+. Strontium, barium, and calcium restored the contractility of the muscle following electrical stimulation when the tissue was in biological fluid absolutely depleted of calcium. These findings suggest that Sr2+ and Ba2+ may be able to substitute Ca2+ in the rat diaphragm for its contractions and nifedipine and diltiazem may follow different mechanisms of actions or channels in their blocking effects.

Effect of nifedipine and amlodipine on wound healing in rats.

The wound healing effect of two calcium channel blockers, nifedipine and amlodipine was studied in rats using incision and excision wound models. In incision wound, two straight paravertebral skin thickness incision were made and on tenth day skin tensile strength was measured by using continuous water flow technique. In excision wound, circular piece of skin excised in its full thickness and wound contraction monitored by alternate day wound tracing and epithelisation period was monitored by noting the number of days required for escher to fall. Drugs enhanced the skin tensile strength in incision wound model. In excision wound model, wound contraction is increased on 4th and 16th day but epithlisation period was not significantly altered. In conclusion, calcium channel blockers can be used to enhance wound healing, especially if wound healing was suppressed by steroids.

Nifedipine potentiates gabapentin antinociception in rats.

To evaluate the involvement of Ca++ channels in Gabapentin antinociception. In healthy male albino rats formalin (50 microliters, 5%) was injected at the planter surface of the paw. Pain score was calculated. Antinociceptive effect of (10, 30 mg/kg) gabapentin and (3, 10 mg/kg) nifedipine alone and on co-administration of sub analgesic doses was studied 30 minutes after formalin injection and reduction in pain scores was calculated. Gabapentin (30 mg/kg) and nifedipine (10 mg/kg) reduced the pain score in formalin injected rats. Gabapentin (10 mg/kg) and nifedipine (3 mg/kg) given alone did not modify pain score, however, on co-administration they significantly reduced the pain score. Study provides evidence of involvement of Ca++ channels in gabapentin antinociception.

Prospective randomized study comparing nifedipine versus ritodrine for the suppression of preterm labour

Nifedipine is a dihydropyridine and a calcium channel blocker during the second phase of the action potential of uterine smooth muscle cells, and ritodrine is a beta-sympathomimetic. Objective of Study: To compare the efficacy and side-effects of oral nifedipine to ritodrine in the inhibition of preterm labour. Methodology: Sixty parturients admitted to the Maternity Hospital with preterm labour who fulfilled the inclusion criteria were randomized into two equal therapy groups: [a] oral nifedipine [n = 30] and [b] intravenous ritodrine [n = 30]. During the period, the parturients were under continuous monitoring of fetal well-being, maternal uterine contractions, blood pressure, and pulse and respiratory rates. Both groups were given dexamethasone and followed up through delivery and the early neonatal period. The incidence of preterm deliveries during the study period was 6.5%. Ritodrine had a quicker onset of inhibition of uterine contractions, especially between 20 and 40 min after initiation of tocolytic therapy [p < 0.04]. Labour was delayed on the average for 40 h in the nifedipine group compared to 24 h in the ritodrine group [p < 0.05]. Eighteen patients [60%] in the nifedipine group had cessation for more than 48 h compared to 7 [30.4%] in the ritodrine group [p < 0.05]. Nifedipine inhibited uterine contractions for more than 7 days in more patients than ritodrine [13 versus 5, p < 0.05]. Ten patients in the nifedipine group went beyond 36 weeks of gestation compared to 4 in the ritodrine group [p < 0.03]. In 5 [17.9%] of the ritodrine group compared to none in the nifedipine group, treatment was abandoned because of severe side-effects of nausea [11 versus 2, p < 0.01] and palpitations [16 versus 3, p < 0.004]. There were no significant differences in the Apgar scores and neonatal morbidity. More infants in the ritodrine group [17, 73.9%] than in the nifedipine group [14, 46.1%, p < 0.05] were admitted to the neonatal unit. Nifedipine is recommended for aborting preterm contractions because it has fewer side-effects, superior efficacy and greater ease of administration than intravenous ritodrine