Adalat scientific update |
|
 |
|
Blood Press. 2007 Mar 1;16 Suppl 1:18-23.
Huo Y, Zhang J, He Q, Chen H, Ma J, Landen H.
Beijing University First Hospital. Beijing. China.
Efficacy and safety of nifedipine GITS in Chinese patients with hypertension - A post-marketing surveillance study.
A post-marketing observation study on the effectiveness and safety of nifedipine GITS in Chinese patients with hypertension .Purpose. This post-marketing surveillance study assessed the efficacy, safety and tolerability of the treatment
with nifedipine GITS (gastro-intestinal therapeutic system) in hypertensive patients under normal daily practice
conditions in China. Patients and methods. A total of 3003 patients were included in 174 outpatient clinics.
Patients received 30 mg or 60 mg of nifedipine GITS. Data were collected at up to three follow-up visits. Results.
At the end of the observation period, mean treatment duration was 13.3 weeks. Mean blood pressure reduction was
27.6/13.6 mmHg, 62.1% of patients had a systolic blood pressure <140 mmHg, and 82.2% had a diastolic blood pressure
<90 mmHg. Blood pressure control according to international guidelines was achieved in 45.0% of all patients. A
total of 1515 patients received additional antihypertensive medications, of which angiotensin-converting enzyme
(ACE) inhibitors were mostly used (42.2%) followed by beta-blockers (33.7%). Twenty-two patients (0.7%) experienced
27 adverse events. Physicians' assessments of efficacy, tolerability and patient acceptance had ratings of "very
good" and "good" in 88.7% (efficacy), 92.8% (tolerability) and 89.1% (patient acceptance) of patients. Conclusions.
Nifedipine GITS proved to be effective and well tolerated for the treatment of hypertension in 3003 Chinese
patients. The results confirm the findings of previously performed clinical studies.
Eur J Pharmacol. 2007 Mar 30;
Esmaeili-Mahani S, Fereidoni M, Javan M, Maghsoudi N, Motamedi F, Ahmadiani A.
Departments of Physiology & Pharmacology, Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Biology, Faculty of Sciences, Shahid Bahonar University, Kerman, Iran.
Nifedipine suppresses morphine-induced thermal hyperalgesia: Evidence for the role of corticosterone.
Morphine-induced thermal hyperalgesia will be suppressed by Nifedipine: a proof for the role of corticosterone.
It has been shown that systemic administration of morphine induced a hyperalgesic response at an extremely low
dose. We have examined the effect of nifedipine, as a calcium channel blocker, on morphine-induced hyperalgesia in
intact and adrenalectomized rats and on hypothalamic-pituitary-adrenal axis activity induced by ultra-low dose of
morphine. To determine the effect of nifedipine on hyperalgesic effect of morphine, nifedipine (2 mg/kg i.p. and 10
mug i.t.) that had no nociceptive effect, was injected concomitant with morphine (1 mug/kg i.p. and 0.01 mug i.t.
respectively). The tail-flick test was used to assess the nociceptive threshold, before and 30, 60, 120, 180, 240
and 300 min after drug administration. The data showed that low dose morphine systemic administration could produce
hyperalgesic effect in adrenalectomized rats equivalent to sham-operated animals while intrathecal injection of
morphine only elicited hyperalgesia in sham-operated animals. Nifedipine could block morphine-induced hyperalgesia
in sham and adrenalectomized rats and even a mild analgesic effect was observed in the adrenalectomized group which
was reversed by corticosterone replacement. Systemic administration of low dose morphine produced significant
increase in plasma level of corticosterone. Nifedipine has an inhibitory effect on morphine-induced corticosterone
secretion. Thus, the data indicate that dihydropyridine calcium channels are involved in ultra-low dose
morphine-induced hyperalgesia and that both the pattern of morphine hyperalgesia and the blockage of it by
nifedipine are modulated by manipulation of the hypothalamic pituitary adrenal axis.
Front Biosci. 2007 May 1;12:2876-89.
von Dadelszen P, Menzies J, Gilgoff S, Xie F, Douglas MJ, Sawchuck D, Magee LA.
Department of Obstetrics and Gynaecology, University of British Columbia and British Columbia Reproductive Care Program, Provincial Health Services Authority, Vancouver, BC, Canada.
Evidence-based management for preeclampsia.
Preeclampsia: evidence-based management. This review reflects both the variable presentation and the systemic nature of preeclampsia. Recommendations for
the comprehensive evaluation and management of organ dysfunction associated with pre-eclampsia are included. The
main points in the review are that: (1) Preeclampsia is a systemic disorder that may affect many organ systems. (2)
For preeclampsia remote from term (<34 weeks), expectant management improves perinatal outcomes, but requires
obsessive surveillance to mitigate maternal risks and is a "package." (3) Initial assessment and ongoing
surveillance of women with preeclampsia should include assessment of all vulnerable maternal organs as well as of
the fetus. (4) Initiate antihypertensive drug treatment immediately if sBP >160 mmHg or dBP more than 110 mmHg, or
if sBP 140-159 mmHg and/or dBP 85-109 mmHg (prepregnancy renal disease or diabetes). (5) The treatment of nonsevere
pregnancy hypertension should include a treatment goal of dBP 80-105 mmHg (depending on practitioner preference),
with one of the following agents, Methyldopa, Labetalol, Nifedipine, or, with special indications (renal or cardiac
diseases), diuretics. (6) Drugs to avoid: angiotensin-converting enzyme inhibitors; angiotensin II receptor
antagonists; and atenolol. (7) For the acute management of severe hypertension, initially reduce dBP by 10 mmHg and
maintain the blood pressure at or below that level with either Nifedipine or Labetalol. (8) For both prophylaxis
against and treatment of eclampsia, MgSO4 (4 g IV stat, then 1 g/hr). (9) For recurrent seizures, MgSO4 (2g IV
stat, then increase to 1.5 g/hr). (10) Total fluid intake should not exceed 80 ml/hr; tolerate urine outputs as low
as 10 ml/hr. (11) Early-onset and/or severe preeclampsia predict later cardiovascular morbidity and mortality; it
would seem prudent to offer such women screening and lipid lowering interventions.
J Huazhong Univ Sci Technolog Med Sci. 2007;27(2):153-6.
Cheng D, Xu Y, Liu X, Zhao L, Xiong S, Zhang Z.
Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
The effects of protein kinase C (PKC) on the tension of normal and passively sensitized human airway smooth muscle and the activity of voltage-dependent delayed rectifier potassium channel (Kv).
The tension of regular and inertly sensitized human airway smooth muscle by the usage of protein kinase C (PKC) and the movement of voltage-dependent delayed rectifier potassium channel (Kv).
The effects of protein kinase C (PKC) on the tension and the activity of voltage-dependent delayed rectifier
potassium channel (K(y)) were examined in normal and passively sensitized human airway smooth muscle (HASM), by
measuring tones and whole-cell patch clamp techniques, and the K(v) activities and membrane potential (E (m)) were
also detected. The results showed that phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a
concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in
asthma serum group was significantly higher than that of the normal group (P<0.05), and the constrictions of both
groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. K(v)
activities of HASM cells were significantly inhibited by PMA, and the E (m) became more positive, as compared with
the DMSO (a PMA menstruum)-treated group (P<0.01). This effect could be blocked by Ro31-8220 (P<0.01). It was
concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced K(v)
activity. In passively sensitized HASM rings, this effect was more notable.
Life Sci. 2007 Apr 21;
Campos-Toimil M, Orallo F.
Departamento de Farmacoloxia, Facultade de Farmacia, Universidade de Santiago de Compostela, Campus Universitario Sur, E-15782 Santiago de Compostela (A Coruna), Spain.
Effects of (-)-epigallocatechin-3-gallate in Ca(2+)-permeable non-selective cation channels and voltage-operated Ca(2+) channels in vascular smooth muscle cells.
How (-)-epigallocatechin-3-gallate affects Ca(2+)-permeable non-selective cation channels and voltage-operated Ca(2+) channels in vascular smooth muscle cells
The effects of (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin of tea, on Ca(2+)-permeable
non-selective cation currents (NSCC) and voltage-operated Ca(2+) channels (VOCC) have been investigated in cultured
rat aortic smooth muscle cells using the whole-cell voltage-clamp technique. Under the Cs(+)/tetraethylammonium
(TEA)-containing internal solution, and in the presence of nifedipine (1 muM), EGCG (30 muM) activated a
long-lasting inward current, with a reversal potential (E(rev)) of approximately 0 mV. This current was not
significantly altered by the replacement of [Cl(-)](i) or [Cl(-)](o), implying that the inward current was not a
chloride channel, but a NSCC. SKF 96365 (30 muM) and Cd(2+) (500 muM) almost completely abolished the EGCG-induced
NSCC. A higher dose of EGCG (100 muM) additionally activated a nifedipine-sensitive inward current in the absence
of depolarization protocol. EGCG (100 muM) also potentiated a nifedipine-sensitive voltage-dependent Ba(2+)-current
during the first 5 min of incubation. However, after > 10 min of incubation with EGCG, this current was
significantly inhibited. Our results suggest that EGCG caused a Ca(2+) influx into smooth muscle cells via VOCC
(probably L-type) and other SKF-96365- and Cd(2+)-sensitive Ca(2+)-permeable channels. The action described here
may be responsible for the contraction induced by EGCG in rat aortic rings and for the rise of the intracellular
concentration of Ca(2+) in rat aortic smooth muscle cells evoked by this catechin. On the other hand, the
inhibition of VOCC after > 10 min of incubation may be, in part, responsible for the relaxation of rat aorta
induced by EGCG.
Eur J Pharm Biopharm. 2006 Aug 26;
Pattarino F, Giovannelli L, Bellomi S.
DISCAFF, School of Pharmacy, University of Piemonte Orientale, Novara, Italy.
Effect of poloxamers on nifedipine microparticles prepared by Hot Air Coating technique.
How poloxamers affect nifedipine microparticles using Hot Air Coating technique?
The Hot Air Coating (HAC) technique was used to prepare microparticles consisting of 30% nifedipine coated with different lipid mixtures. Cetearyl alcohol or cetearyl alcohol and 5% or 15% of a poloxamer (Pluronic F68 or Pluronic F127) were used as excipients. HAC products were analyzed in terms of morphology, flowability, thermal properties and nifedipine release behaviour, in order to elucidate the role played by the Pluronics on the physico-chemical and pharmaceutical characteristics of microparticles. HAC particles were spherical and their surface appeared scale-worked; thermal studies demonstrated the existence of relevant interactions among the system components and the dissolution experiments led to the hypothesis that the drug is released primarily by diffusion through the lipid coating: the poloxamer and its concentration have a significant influence on the pharmaceutical properties of the dosage form, as shown by the a parameter of Weibull model.
Health Technol Assess. 2005 Aug;9(30):iii-vi, xiii-163.
Newman DJ, Mattock MB, Dawnay AB, Kerry S, McGuire A, Yaqoob M, Hitman GA, Hawke C.
South-West Thames Institute for Renal Research, St Helier Hospital, Carshalton, UK.
Systematic review on urine albumin testing for early detection of diabetic complications.
Check urine albumin on regular basis for the early detection of diabetic complications.
OBJECTIVES: To determine whether microalbuminuria is an independent prognostic factor for the development of diabetic complications and whether improved glycaemic or blood pressure control has a greater influence on the development of diabetic complications in those with microalbuminuria than in those with normoalbuminuria. DATA SOURCES: Electronic databases up until January 2002. REVIEW METHODS: A protocol for peer review by an external expert panel was prepared that included selection criteria for data extraction and required two independent reviewers to undertake article selection and review. Completeness was assessed using hand-searching of major journals. Random effects meta-analysis was used to obtain combined estimates of relative risk (RR). Funnel plots, trim and fill methods and meta-regression were used to assess publication bias and sources of heterogeneity. RESULTS: In patients with type 1 or type 2 DM and microalbuminuria there is a RR of all-cause mortality of 1.8 [95% confidence interval (CI) 1.5 to 2.1] and 1.9 (95% CI 1.7 to 2.1) respectively. Similar RRs were found for other mortality end-points, with age of cohort being inversely related to the RR in type 2 DM. In patients with type 1 DM, there is evidence that microalbuminuria or raised albumin excretion rate has only weak, if any, independent prognostic significance for the incidence of retinopathy and no evidence that it predicts progression of retinopathy, although strong evidence exists for the independent prognostic significance of microalbuminuria or raised albumin excretion rate for the development of proliferative retinopathy (crude RR of 4.1, 95% CI 1.8 to 9.4). For type 2 DM, there is no evidence of any independent prognostic significance for the incidence of retinopathy and little, if any, prognostic relationship between microalbuminuria and the progression of retinopathy or development of proliferative retinopathy. In patients with type 1 DM and microalbuminuria there is an RR of developing end-stage renal disease (ESRD) of 4.8 (95% CI 3.0 to 7.5) and a higher RR (7.5, 95% CI 5.4 to 10.5) of developing clinical proteinuria, with a significantly greater fall in glomerular filtration rate (GFR) in patients with microalbuminuria. In patients with type 2 DM, similar RRs were observed: 3.6 (95% CI 1.6 to 8.4) for developing ESRD and 7.5 (95% CI 5.2 to 10.9) for developing clinical proteinuria, with a significantly greater decline in GFR in the microalbuminuria group of 1.7 (95% CI 0.1 to 3.2) ml per minute per year compared with those who were normoalbuminuric. In adults with type 1 or type 2 DM and microalbuminuria at baseline, the numbers progressing to clinical proteinuria (19% and 24%, respectively) and those regressing to normoalbuminuria (26% and 18%, respectively) did not differ significantly. In children with type 1 DM, regression (44%) was significantly more frequent than progression (15%). In patients with type 1 or type 2 DM and microalbuminuria, there is scarce evidence as to whether improved glycaemic control has any effect on the incidence of cardiovascular disease (CVD), the incidence or progression of retinopathy, or the development of renal complications. However, among patients not stratified by albuminuria, improved glycaemic control benefits retinal and renal complications and may benefit CVD. In the effects of angiotensin-converting enzyme (ACE) inhibitors on GFR in normotensive microalbuminuric patients with type 1 DM, there was no evidence of a consistent treatment effect. There is strong evidence from 11 trials in normotensive type 1 patients with microalbuminuria of a beneficial effect of ACE inhibitor treatment on the risk of developing clinical proteinuria and on the risk of regression to normoalbuminuria. Patients with type 2 DM and microalbuminuria, whether hypertensive or not, may obtain additional cardiovascular benefit from an ACE inhibitor and there may be a beneficial effect on the development of retinopathy in normotensive patients irrespective of albuminuria. There is limited evidence that treatment of hypertensive microalbuminuric type 2 diabetic patients with blockers of the renin--angiotensin system is associated with preserved GFR, but also evidence of no differences in GFR in comparisons with other antihypertensive agents. The data on GFR in normotensive cohorts are inconclusive. In normotensive type 2 patients with microalbuminuria there is evidence from three trials (all enalapril) of a reduction in risk of developing clinical proteinuria; in hypertensive patients there is evidence from one placebo-controlled trial (irbesartan) of a reduction in this risk. Intensive compared with moderate blood pressure control did not affect the rate of progression of microalbuminuria to clinical proteinuria in the one available study. There is inconclusive evidence from four trials of any difference in the proportions of hypertensive patients progressing from microalbuminuria to clinical proteinuria when ACE inhibitors are compared with other antihypertensive agents, and in one trial regression was two-fold higher with lisinopril than with nifedipine. CONCLUSIONS: The most pronounced benefits of glycaemic control identified in this review are on retinal and renal complications in both normoalbuminuric and microalbuminuric patients considered together, with little or no evidence of any greater benefit in those with microalbuminuria. Hence, microalbuminuric status may be a false boundary when considering the benefits of glycaemic control. Classification of a person as normoalbuminuric must not serve to suggest that they will derive less benefit from optimal glycaemic control than a person who is microalbuminuric. All hypertensive patients benefit from blood pressure lowering and there is little evidence of additional benefit in those with microalbuminuria. Antihypertensive therapy with an ACE inhibitor in normotensive patients with microalbuminuria is beneficial. Monitoring microalbuminuria does not have a proven role in modulating antihypertensive therapy while the patient remains hypertensive. Recommendations for microalbuminuria research include: determining rate and predictors of development and factors involved in regression; carrying out economic evaluations of different screening strategies; investigating the effects of screening on patients; standardising screening tests to enable use of common reference ranges; evaluating the effects of lipid-lowering therapy; and using to modulate antihypertensive therapy.
BJOG. 2005 Mar;112 Suppl 1:79-83.
Geijn HP, Lenglet JE, Bolte AC.
Department of Obstetrics and Gynaecology, Vrije Universiteit Medical Center (VUmc), De Boelelaan, Amsterdam, The Netherlands.
Nifedipine trials: effectiveness and safety aspects.
Effectiveness and safety aspects of Nifedipine trials.
Nifedipine (Adalat) is marketed as an anti-hypertensive agent. Nifedipine inhibits voltage-dependent L-type calcium channels, which leads to vascular (and other) smooth muscle relaxation and negative inotropic and chronotropic effects on the heart. Vasodilation, followed by a baroreceptor-mediated increase in sympathetic tone then results in indirect cardiostimulation. Nifedipine was introduced as a tocolytic agent at a time when beta-agonists and magnesium sulphate dominated the arena for the prevention of preterm birth. The oral administration route, the availability of immediate and slow-release preparations, the low incidence of (mild) side effects, and its limited costs explain the attraction to this medication from the obstetric field and its rapid and widespread distribution. Currently, over 40 studies have been published on nifedipine's tocolytic effectiveness, including seven meta-analyses. The quality of the studies suffers particularly from performance bias because the majority of them failed to ensure adequate blinding to treatment both for providers and patients. Concerns about other methodological flaws include measurements, outcome assessment and attrition bias. In particular, the safety aspects of nifedipine for tocolysis have been underassessed. Conclusions from the meta-analyses, favouring the use of nifedipine as a tocolytic agent, are not supported by close examination of the data. The tocolytic effectiveness and 'safety' of nifedipine has been studied primarily in normal pregnancies. Based on its pharmacological properties, one should be cautious to administer nifedipine when the maternal cardiovascular condition is compromised, such as with intrauterine infection, twin pregnancy, maternal hypertension, cardiac disease, etc. Life-threatening pulmonary oedema and/or cardiac failure are definite risks and have been reported. Under such circumstances, the baroreceptor-mediated increase in sympathetic tone may not balance the cardiac-depressant activity of nifedipine.
Adalat description...
|
|
Drug category:Hypotensive agents
 Adalat scientific update
Buy here
|
|
My Basket