Tag: M.W=200-350

Cox, Annie G. published the artcileCurrent and emerging pharmacotherapy for emergency management of preeclampsia, COA of Formula: C17H18N2O6, the main research area is preeclampsia emerging pharmacotherapy review; Preeclampsia; antihypertensives; eclampsia; mortality; pregnancy.

: Preeclampsia is a disease specific to pregnancy characterised by new onset hypertension with maternal organ dysfunction and/or fetal growth restriction. It remains a major cause of maternal and perinatal morbidity and mortality. For fifty years, antihypertensives have been the mainstay of treating preeclampsia, reducing maternal morbidity and mortality. With increased knowledge of the mechanisms underlying the disease has come opportunities for novel therapies that complement antihypertensives by protecting the maternal vasculature.: In this review, the authors consider, in detail, the antihypertensives commonly used today in the emergency care of women with severe preeclampsia. They also review less common anti-hypertensive agents and discuss the role of magnesium sulfate in the management of preeclampsia and the prevention of eclampsia. Finally, they explore novel therapeutics for the acute management of preeclampsia.: The rapid control of maternal hypertension will, and must, remain the mainstay of emergency treatment for women with severe preeclampsia. The role of magnesium sulfate as a primary prevention for eclampsia is context dependant and should not displace a focus on correcting blood pressure safely. The exploration of novel adjuvant therapies will likely allow us to prolong pregnancy longer and improve perinatal outcomes safely for the mother.

Expert Opinion on Pharmacotherapy published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, COA of Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Martin, Courtney published the artcileSemiautonomous Treatment Algorithm for the Management of Severe Hypertension in Pregnancy, Computed Properties of 21829-25-4, the main research area is pregnancy severe hypertension semiautonomous treatment algorithm management.

To evaluate whether implementation of a semiautonomous treatment algorithm was associated with improved compliance with American College of Obstetricians and Gynecologists guidelines for rapid administration of antihypertensive therapy in the setting of sustained severe hypertension. This was a single-center retrospective cohort study of admitted pregnant and postpartum patients treated for severe hypertension between Jan. 2017 and March 2020. The semiautonomous treatment algorithm, which included vital sign monitoring, blood pressure thresholds for diagnosis of severe hypertension, and automated order sets for recommended first-line antihypertensive therapy were implemented between May 2018 and March 2019. The primary outcomes were the administration of antihypertensive therapy within 15, 30 and 60 min of diagnosis of severe hypertension. Comparisons were made between the preimplementation, during implementation, and postimplementation groups using χ2. Anal. was limited to the first episode of severe hypertension treated. Statistical significance was defined as P<.05. In total, there were 959 obstetric patients treated for severe hypertension, with 373 (38.9%) treated preimplementation, 334 (34.8%) during implementation, and 252 (26.2%) after implementation. Treatment of severe hypertension within 15 min was 36.5% preimplementation, 45.8% during implementation, and 55.6% postimplementation (P = .001). Treatment within 30 min was 65.9% in the preimplementation group, 77.8% during implementation, and 79.0% in the postimplementation group (P = .004). There was no difference in percentage of patients treated within 60 min (86.3% before, 87.7% during and 92.9% after implementation, P = .12). Implementation of a semiautonomous treatment algorithm for severe hypertension was associated with a higher percentage of pregnant and postpartum patients receiving the first dose of antihypertensive therapy within 15 and 30 min. Implementation of similar algorithms for this and other obstetric indications may decrease time to appropriate therapy and help improve care equity. Obstetrics & Gynecology (Philadelphia, PA, United States) published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Computed Properties of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Zulfeen, Momina published the artcileIV labetalol and oral nifedipine in acute control of severe hypertension in pregnancy-A randomized controlled trial, Category: pyridine-derivatives, the main research area is hypertension pregnancy labetalol nifedipine intravenous oral drug delivery system; Hypertension; Labetalol; Nifedipine; Preeclampsi; Pregnancy.

We conducted a parallel double-blinded randomized controlled trial between Dec. 2014 to Dec. 2016 in 120 antenatal women of gestational age >28 wk, admitted with severe hypertension of blood pressure â‰?60/110 mm Hg to maternity ward at a tertiary hospital. The labetalol group received 20 mg initially followed by escalating doses of 40 mg, 80 mg, 80 mg and 80 mg (5 doses) every 15 min to a maximum of 300 mg. Nifedipine group received 10 mg initially followed by repeated doses of 20 mg every 15 min (total 5 doses) to a maximum of 90 mg. Vital signs were recorded every 15 min.-The time taken and the number of doses required to achieve the target blood pressure (150/100 mmHg). Survival anal. was used to compare the efficacy of treatment regimens. Sixty women were randomised to each group and none were lost to follow-up. None of the patients in nifedipine group required labetalol, whereas three patients in labetalol group achieved target BP only after receiving nifedipine was administered after the maximum dose of labetalol. The mean time taken to achieve the target blood pressure in the labetalol group was higher (36.75 min) than in the nifedipine group (27.25 min) [mean difference 9.5 min,p = 0.002]. Nifedipine group required significantly lower doses (1.82 ± 0.83) as compared to labetalol (2.45 ± 1.32) [p = 0.002]. Nifedipine was 1.8 times more likely to achieve target blood pressure (Hazard Ratio = 1.8).

European Journal of Obstetrics & Gynecology and Reproductive Biology published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Vaibavi, S. R. published the artcileCalcium-channel-blockers exhibit divergent regulation of cancer extravasation through the mechanical properties of cancer cells and underlying vascular endothelial cells, Synthetic Route of 21829-25-4, the main research area is calcium channel blocker cancer vascular endothelial cell; Calcium channel blockers; Membrane-viscoelasticity.; Migration; Morphology; Optical Tweezer; TEER; Traction stress.

Cardiovascular and cancer illnesses often co-exist, share pathol. pathways, and complicate therapy. In the context of the potential oncol. role of cardiovascular-antihypertensive drugs (AHD), here we examine the role of calcium-channel blocking drugs on mechanics of extravasating cancer cells, choosing two clin.-approved calcium-channel blockers (CCB): Verapamil-hydrochloride and Nifedipine, as model AHD to simultaneously target cancer cells (MCF7 and or MDA231) and an underlying monolayer of endothelial cells (HUVEC). First, live-cell microscopy shows that exposure to Nifedipine increases the spreading-area, migration-distance, and frequency of transmigration of MCF-7 cells through the HUVEC monolayer, whereas Verapamil has the opposite effect. Next, impedance-spectroscopy shows that for monolayers of either endothelial or cancer cells, Nifedipine-treatment alone decreases the impedance of both cases, suggesting compromised cell-cell integrity. Furthermore, upon co-culturing MCF-7 on the HUVEC monolayers, Nifedipine-treated MCF-7 cells exhibit weaker impedance than Verapamil-treated MCF-7 cells. Following, fluorescent staining of CCB-treated cytoskeleton, focal adhesions, and cell-cell junction also indicated that Nifedipine treatment diminished the cell-cell integrity, whereas verapamil treatment preserved the integrity. Since CCBs regulate intracellular Ca2+, we next investigated if cancer cell′s exposure to CCBs regulates calcium-dependent processes critical to extravasation, specifically traction and mechanics of plasma membrane. Towards this end, first, we quantified the 2D-cellular traction of cells in response to CCBs. Results show that exposure to F-actin depolymerizing drug decreases traction stress significantly only for Nifedipine-treated cells, suggesting an actin-independent mechanism of Verapamil activity. Next, using an optical tweezer to quantify the mechanics of plasma membrane (PM), we observe that under constant, externally-applied tensile strain, PM of Nifedipine-treated cells exhibits smaller relaxation-time than Verapamil and untreated cells. Finally, actin depolymerization significantly decreases MSD only for Verapamil treated cancer-cells and endothelial cells and not for Nifedipine-treated cells. Together, our results show that CCBs can have varied, mechanics-regulating effects on cancer-cell transmigration across endothelial monolayers. A judicious choice of CCBs is critical to minimizing the pro-metastatic effects of antihypertension therapy.

Cell Biochemistry and Biophysics published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Synthetic Route of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kristin, Erna published the artcileAntihypertensive drug use after a new drug formulary implementation in a private hospital in Indonesia, Product Details of C17H18N2O6, the main research area is hypertension generic antihypertensive drug formulary Indonesia.

There are many antihypertensive drugs available, but the drugs that have been proven to reduce cardiovascular events should be preferred. This study aims to assess antihypertensive drug prescribing after the implementation of a new drug formulary in a private hospital in Indonesia. This cross-sectional study was conducted on 345 patients with hypertension in a private hospital in Indonesia. Antihypertensive drug use data in the period after the implementation of a new drug formulary (2013-2015) were extracted from the hospital medical records. The characteristics of the prescriptions, the name and pharmacol. classification of the antihypertensive drugs prescribed, types of combination antihypertensive drugs and consistency with the Indonesian National Formulary were assessed. This study included 345 hypertensive patients with 1126 prescriptions containing 3292 drugs. There were 35.4% antihypertensive drug prescriptions, with 3.6% prescriptions containing antihypertensive drug combinations. Calcium channel blockers (74.8%) were most commonly prescribed, with amlodipine as the most common drug name prescribed. A most prevalent antihypertensive drug used in combination was hydrochlorothiazide and captopril (47.5%). All antihypertensive drugs were consistent with the Indonesian National Formulary. In conclusion, The pattern of antihypertensive drug use after the implementation of an evidence-based hospital formulary showed a trend of a better and more rational use of antihypertensive drugs.

Journal of Pharmaceutical Sciences and Research published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Product Details of C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Wang, Hao published the artcileMechanism of contractile dysfunction induced by serotonin in coronary artery in spontaneously hypertensive rats, HPLC of Formula: 21829-25-4, the main research area is rottlerin U73122 Y27632 cardioprotectant serotonin coronary artery vasoconstriction hypertension; 5-HT; Coronary artery; Hypertension; Spontaneously hypertensive rats; Vasoconstriction.

Abstract: Hypertension is one of the risk factors for coronary heart disease. The present study investigated the mechanism of contractile dysfunction induced by serotonin (5-HT) in coronary artery in spontaneously hypertensive rats (SHRs). Coronary arteries were isolated form SHRs and Wistar rats. Arterial ring contraction was measured using a multi myograph system. Intracellular calcium concentration was measured with a Ca2+ probe fluo-4/AM in vascular smooth muscle cells (VSMCs) isolated from coronary arteries. Signaling pathway-related proteins were assayed by western blotting. A 5-HT2A receptor blocker, sarpogrelate, completely eliminated coronary artery contraction induced by 5-HT. PLCβ inhibitor U73122 also significantly inhibited the response to 5-HT. Compared with the Wistar rats, serotonin (5-HT)- and CaCl2-induced coronary vasoconstriction in the SHRs was significantly reduced. Rho-associated protein kinase inhibitor Y27632, PKC inhibitor rottlerin, and L-type calcium channel blocker nifedipine inhibited the 5-HT-induced coronary artery contraction in a dose-dependent manner in SHRs and Wistar rats. However, the inhibitory effects were reduced in SHRs. In addition, store-operated Ca2+ (SOC) induced an obvious Ca2+ influx in coronary arterial smooth muscle cells, whereas SOC-mediated contraction was very slight in coronary arteries. At the same time, it was found that 5-HT2AR, IP3R, and Cav1.2 protein expression and PKCδ activity were decreased, and STIM1 and Orai1 were increased in VSMCs from coronary arteries of SHRs compared with Wistar rats. These results implicate calcium-handling dysfunction mediated by the 5-HT2A receptor and downstream signaling pathway might lead to a reduction in 5-HT-induced contraction in SHR coronary arteries.

Naunyn-Schmiedeberg’s Archives of Pharmacology published new progress about 5-HT2A antagonists. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, HPLC of Formula: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Leal-Junior, Carlos C. published the artcileEffectiveness of an oral versus sublingual loading dose of nifedipine for tocolysis, HPLC of Formula: 21829-25-4, the main research area is nifedipine tocolytic oral sublingual drug delivery premature labor; Nifedipine; Oral administration; Pregnant; Premature; Premature labor; Sublingual administration; Tocolysis.

Objective : To determine the effectiveness of an oral vs. sublingual loading dose of nifedipine for tocolysis. Methods : An open, randomized clin. trial conducted between March 1, 2013, and Apr. 31, 2014. Participants were pregnant women with a diagnosis of premature labor, single live fetus, topical pregnancy, gestational age 24-36 wk, normal fetal vitality, cervical dilatation less than or equal to 4 cm, cervical effacement less than or equal to 80%, and intact amniotic membranes. They were randomized into two groups, oral and sublingual nifedipine, 20 mg loading dose, repeated every 30 min (maximum dose of 60 mg). The primary endpoint was the time until tocolysis and the secondary endpoints were the effectiveness of tocolysis within 90 min, 12 h, and 48 h; premature delivery within 48 h; and maternal hemodynamic parameters and side effects. Results : There were 80 patients randomized to oral (n=40) and sublingual (n=40) nifedipine. The time required for tocolysis was significantly less with sublingual nifedipine (160 min vs 340 min; P=0.0003). Sublingual nifedipine was also more successful than oral nifedipine at inhibiting premature labor within 90 min (n=8 [20.0%] vs n=1 [2.5%], P=0.014). There was no statistically significant difference between the groups for the other secondary endpoints. Conclusion : Compared with oral administration, a sublingual loading dose of nifedipine resulted in faster tocolysis in patients with premature labor. Brazilian Clin. Trials Registry (ReBEC): U1111-11566186.

International Journal of Gynecology & Obstetrics published new progress about Amnion, epithelium. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, HPLC of Formula: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Faconti, Luca published the artcileArterial stiffness can be modulated by pressure-independent mechanisms in hypertension, Category: pyridine-derivatives, the main research area is blood pressure hypertension pulse wave velocity stiffness; autonomic nervous system; high blood pressure; hypertension; pulse wave velocity; stiffness.

Effects of short-term interventions on large-artery stiffness assessed by pulse wave velocity (PWV) have mainly been explained by concomitant changes in blood pressure (BP). However, lower body neg. pressure, which increases sympathetic activity and has other hemodynamic effects, has a specific effect on PWV in healthy volunteers. We examined effects of lower-limb venous occlusion (LVO), a similar intervention to lower-body neg. pressure that reduces BP but increases sympathetic activity and device-guided breathing (DGB), which reduces both BP and sympathetic activity, on PWV in patients with essential hypertension (n = 70 after LVO, n = 45 after DGB and LVO in random order). The short-acting calcium channel antagonist nifedipine was used as a control for changes in BP. LVO produced a small but significant reduction in mean arterial pressure of 1.8 (95% CI 0.3-3.4) mm Hg. Despite this, aortic and carotid-femoral PWV increased during LVO by 0.8 (0.2-1.4) m/s and 0.7 (0.3-1.05) m/s, resp. DGB reduced PWV by 1.2 (0.9-1.4) m/s, to a greater extent than did nifedipine 10 mg (reduction of 0.7 [0.1-1.3] m/s, P<0.05 compared with reduction during DGB). This occurred despite a greater decrease in BP with nifedipine compared with DGB. Arterial stiffness can be modulated independently of BP over the short term. The mechanism could involve alterations in sympathetic activity or other as yet uncharacterized effects of LVO and DGB. Journal of the American Heart Association published new progress about Arterial stiffness. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Sueda, Shozo published the artcileSpasm provocation tests under medication may help decide on medical or mechanical therapy in patients with aborted sudden cardiac death due to coronary spasm, Product Details of C17H18N2O6, the main research area is aborted sudden cardiac death coronary spasm; aborted sudden cardiac death; coronary artery spasm; implantable cardioverter-defibrillator; medications; ventricular fibrillation.

Objective The decision to perform medical or mech. therapy in patients with aborted sudden cardiac death (ASCD) due to coronary spasm is controversial. The Japanese Circulation Society guidelines for the diagnosis and treatment of patients with coronary spastic angina mentioned that implantable cardioverterdefibrillator (ICD) is one option in patients with ASCD due to coronary spasm. We investigated the usefulness of spasm provocation tests under medications in five patients with ASCD due to coronary spasm. Methods We performed the spasm provocation tests under medications in five ASCD patients due to coronary spasm. Pharmacol. spasm provocation tests, including five acetylcholine (ACh) tests, two ergonovine (ER) tests, and two ACh added after ER tests, were performed to estimate the effect of medications to suppressing the next fatal spasms. Results ACh tests under medications did not provoke spasm in one patient but did provoke in two patients. In the remaining two patients, neither the ACh test nor the ER test provoked spasm, but the ACh added after ER test induced a focal spasm in one coronary artery. We increased the medication dosage in four patients. An ICD was implanted in two patients, including one with refractory spasm and one with left main trunk spasm. One patient died due to pulseless elec. activity without ventricular fibrillation, while the remaining four patients survived. Conclusion Spasm provocation tests under medication in patients with ASCD due to coronary spasm may be an option when deciding on medical or mech. therapy.

Internal Medicine (Tokyo, Japan) published new progress about Bioelectric charge. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Product Details of C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kokova, Vesela Yu. published the artcileEtifoxine does not impair muscle tone and motor function in rats as assessed by in vivo and in vitro methods, Related Products of pyridine-derivatives, the main research area is Etifoxine impair muscle tone motor rats.

The purpose of our study is to evaluate the effects of the translocator protein (TSPO) ligand etifoxine on muscle tone and locomotor activity. In addition, the mechanism of action of etifoxine on the presynaptic membrane and neuromuscular junction is investigated. These effects of etifoxine were examined employing the following methods: 1 in vivo experiments using bar holding test and activity cage test, and 2 comparative in vitro studies with nifedipine on indirectly-elicited twitches of striated abdominal muscle preparations Etifoxine in doses 50 mg/kg and 100 mg/kg i.p. does not produce any significant changes in locomotor activity and muscle tone of intact rats. Nifedipine (10-5 M) induces a significant decrease in the muscle force of striated muscle preparations Etifoxine (10-8-10-4 M) has no significant effect on indirectly-elicited twitch tension. Results show that the TSPO ligand etifoxine has no myorelaxant effect. The activation of TSPO is not associated with a reduction in muscle tone and motor impairment. Etifoxine does not affect the presynaptic membrane and its influence on L-type Ca2+-channels is insignificant. Etifoxine does not act as a competitive antagonist of acetylcholine and does not impair the impulse transmission in the neuromuscular junction.

General Physiology and Biophysics published new progress about Locomotor behavior. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Related Products of pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem