Tag: M.W=200-350

Mitsui, Retsu published the artcileRole of K+ channels in maintaining the synchrony of spontaneous Ca2+ transients in the mural cells of rat rectal submucosal arterioles, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is potassium channel calcium mural cell rectal precapillary arteriole; Intercellular synchrony; K+ channels; Microvasculature; Mural cells; Spontaneous Ca2+ transient.

Mural cells in precapillary arterioles (PCAs) generate spontaneous Ca2+ transients primarily arising from the periodic release of Ca2+ from sarcoendoplasmic reticulum (SR/ER). The Ca2+ release induces Ca2+-activated chloride channel (CaCC)-dependent depolarisations that spread to neighboring mural cells to develop the synchrony of their Ca2+ transients. Here, we explored the roles of K+ channels in maintaining the synchrony of spontaneous Ca2+ transients. Intracellular Ca2+ dynamics in mural cells were visualised by Cal-520 fluorescence Ca2+ imaging in the submucosal PCAs of rat rectum. Increasing extracellular K+ concentration ([K+]o) from 5.9 to 29.7 mM converted synchronous spontaneous Ca2+ transients into asynchronous, high-frequency Ca2+ transients. Similarly, the blockade of inward rectifier K+ (Kir) channels with Ba2+ (50μM) or Kv7 voltage-dependent K+ (Kv7) channels with XE 991 (10μM) disrupted the synchrony of spontaneous Ca2+ transients, while the blockers for large-, intermediate- or small-conductance Ca2+-activated K+ channels had no effect. Kir2.1 immunoreactivity was detected in the arteriolar endothelium but not mural cells. In the PCAs that had been pretreated with XE 991 or Ba2+, nifedipine (1μM) attenuated the asynchronous Ca2+ transients but failed to restore their synchrony. In contrast, levcromakalim, an ATP-sensitive K+ channel opener, restored the synchronous Ca2+ transients. Thus, constitutively active Kv7 and Kir channels appear to be involved in maintaining the relatively hyperpolarised membrane of mural cells. The hyperpolarised membrane prevents depolarisation-induced ‘premature’ Ca2+ transients to ensure sufficient SR/ER Ca2+ refilling that is required for regenerative Ca2+ release resulting in synchronous Ca2+ transients amongst the mural cells.

Pfluegers Archiv published new progress about Arterial endothelium, arteriolar endothelium (precapillary). 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, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Zhang, Jinggui published the artcileEfficacy and safety of combination of magnesium sulfate, phentolamine and nifedipine in treatment of patients with hypertensive disorder complicating pregnancy, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is magnesium sulfate phentolamine nifedipine hypertensive disorder pregnancy; hemodynamics; hypertensive disorder complicating pregnancy; magnesium sulfate; nifedipine; phentolamine; urinary protein.

Efficacy and safety of the combination of magnesium sulfate, phentolamine and nifedipine in the treatment of patients with hypertensive disorder complicating pregnancy (HDCP) and its effect on hemodynamics and urinary protein level were investigated. One hundred and six patients with HDCP diagnosed at the Affiliated Hospital of Beihua University from Feb. 5, 2016 to May 9, 2017 were retrospectively analyzed. Patients were divided into the magnesium sulfate group and the combination group, according to the therapeutic schemes. The efficacy 1 wk later was observed The general clin. data of the patients were recorded, and data were acquired with respect to hemodynamic indexes before and after treatment [changes of S/D ratio of umbilical artery flow, and cardiac index and total peripheral resistance (TPR)], the 24-h urinary protein level, clin. efficacy and safety [adverse drug reactions (ADR) and maternal and neonatal outcomes]. Before treatment, there was no statistically significant difference between the two groups in terms of S/D ratio of umbilical artery flow (P>0.05), while after treatment the S/D ratio was significantly lower than that before treatment in both groups (P<0.05). Before treatment, there was no statistically significant difference between the two groups in terms of cardiac index (P>0.05). TPR after treatment was significantly lower than that before treatment in both groups (P<0.001). Compared with the magnesium sulfate group, patients in the combination group had significantly lower 24-h urinary protein level after treatment (P<0.001), significantly higher total effective rate (P<0.05), significantly lower incidence rate of ADR (P<0.001), and significantly lower incidence rate of adverse maternal and neonatal outcomes (P<0.001). In conclusion, the combination of magnesium sulfate, phentolamine and nifedipine can significantly improve the hemodynamic indexes, the 24-h urinary protein level, the clin. efficacy, ADR and maternal and neonatal outcomes of patients with HDCP, therefore it is worthy of use in the clinic. Experimental and Therapeutic Medicine published new progress about Cardiovascular system. 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, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Yilmaz, Osman published the artcileEffects of nifedipine on fetal cardiac function in preterm labor, Formula: C17H18N2O6, the main research area is mitral valve fetus preterm labor nifedipine; fetal cardiac functions; myocardial performance index; nifedipine; preterm labor; sphericity index.

To evaluate the effects of nifedipine treatment on fetal hemodynamics and cardiac function during preterm labor. This prospective study assessed several quant. parameters of fetal cardiac circulation and function, and found no significant changes at 48 h after nifedipine treatment. These findings suggest that tocolytic nifedipine may be safe for fetuses. It supports clinicians to use nifedipine treatment for tocolysis without any cardiac effect on the fetus. A prospective cohort study was conducted at a tertiary hospital between Jan. 2016 and Oct. 2017. A total of 45 pregnant women who required nifedipine for preterm labor were included in this study. Fetal Doppler ultrasound was performed and fetal systolic and diastolic function was measured prior to, and 48 h after, the first nifedipine treatment. Conventional Doppler parameters were used to evaluate fetal heart function and hemodynamic changes. Tricuspid annular plane systolic excursion, mitral annular plane systolic excursion and the sphericity index were also evaluated to assess changes in fetal cardiac morphol. No significant changes in fetal Doppler parameters were observed following nifedipine tocolysis. There was no significant difference in the fetal cardiac function parameters of both ventricles before vs. after nifedipine treatment. Tricuspid annular plane systolic excursion, mitral annular plane systolic excursion, and sphericity index values were unchanged following nifedipine treatment.

Journal of Perinatal Medicine published new progress about Cardiovascular system. 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, Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Franze, Silvia published the artcileDrug-in-micelles-in-liposomes (DiMiL) systems as a novel approach to prevent drug leakage from deformable liposomes, COA of Formula: C17H18N2O6, the main research area is micelles liposome drug delivery systems; Elastic vesicles; Ethosomes; Nifedipine; Piroxicam; Transdermal; Transethosomes; Transfersomes.

Deformable liposomes (DL) are successfully exploited to enhance the skin penetration of several compounds Nevertheless, the “”soft”” nature of the bilayer favors the drug leakage, mainly in the case of hydrophobic compounds This work aimed to develop a suitable strategy to stabilize the lipid bilayer, without compromising the deformability properties of DL. The approach relied on the design of a “”matryoshka”” system, namely a drug in micelles in deformable liposomes (DiMiL) system. The performances (drug leakage, deformability and in vitro skin penetration profile) of DiMiLs were tested using nifedipine and piroxicam as model compounds and compared to those of traditional DL. The micelles were made of Kolliphor HS15 whereas the lipid vesicles were composed of egg-phosphatidylcholine and Tween 80 (T80) at 95:5 or 85:15 weight/weight ratios. As expected, the drug leakage from DL was high after only one month of storage (almost 50% in the case of nifedipine and in the range of 39-79% in the case of piroxicam loaded DL, depending on T80 content). Optimized DiMiL formulations retained instead the drug content up to two-months storage period. Moreover, the constant of deformability of DiMiLs felt in the acceptance range for deformable vesicles intended for cutaneous application and the skin permeated amount of the delivered drugs was increased of at least 4 times. In conclusion, DiMiL reveals to be a suitable approach to avoid the leakage of hydrophobic compounds and an attractive transdermal drug delivery system for poorly permeable drugs.

European Journal of Pharmaceutical Sciences published new progress about Drug delivery systems. 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

Oikonomou, Katerina D. published the artcileCalcium dysregulation and compensation in cortical pyramidal neurons of the R6/2 mouse model of Huntington′s disease, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is Huntington disease calcium dysregulation cortical pyramidal neuron; Huntington’s disease; R6/2 mice; calcium imaging; cortical pyramidal neurons; dantrolene; two-photon laser scanning microscopy.

Huntington′s disease (HD) is a fatal, hereditary neurodegenerative disorder that predominantly affects striatal medium-sized spiny neurons and cortical pyramidal neurons (CPNs). It has been proposed that perturbations in Ca2+ homeostasis could play a role in CPN alterations. To test this hypothesis, we used the R6/2 mouse model of juvenile HD at different stages of disease progression; presymptomatic, early symptomatic, and late symptomatic. We combined whole-cell patch-clamp recordings of layer 2/3 CPNs with two-photon laser scanning microscopy to image somatic and dendritic Ca2+ transients associated with evoked action potentials (APs). We found that the amplitude of AP-induced Ca2+ transients recorded at the somata of CPNs was significantly reduced in presymptomatic and late symptomatic R6/2 mice compared with wild-type (WT) littermates. However, reduced amplitudes were compensated by increases in decay times, so that Ca2+ transient areas were similar between genotypes. AP-induced Ca2+ transients in CPN proximal dendrites were variable and differences did not reach statistical significance, except for reduced areas in the late symptomatic group. In late symptomatic mice, a specific store-operated Ca2+ channel antagonist, EVP4593, reduced somatic Ca2+ transient amplitude similarly in WT and R6/2 CPNs. In contrast, dantrolene, a ryanodine receptor (RyR) antagonist, and nifedipine, an L-type Ca2+ channel blocker, significantly reduced both somatic Ca2+ transient amplitude and area in R6/2 but not WT CPNs. These findings demonstrate that perturbations of Ca2+ homeostasis and compensation occur in CPNs before and after the onset of overt symptoms, and suggest RyRs and L-type Ca2+ channels as potential targets for therapeutic intervention. NEW & NOTEWORTHY We used two-photon microscopy to examine calcium influx induced by action potentials in cortical pyramidal neurons from a mouse model of Huntington′s disease (HD), the R6/2. The amplitude of somatic calcium transients was reduced in R6/2 mice compared with controls. This reduction was compensated by increased decay times, which could lead to reduced calcium buffering capacity. L-type calcium channel and ryanodine receptor blockers reduced calcium transient area in HD neurons, suggesting new therapeutic avenues.

Journal of Neurophysiology published new progress about Animal cell, somatic. 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, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Estrada-Soto, Samuel published the artcileAntihypertensive and vasorelaxant mode of action of the ethanol-soluble extract from Tagetes lucida Cav. aerial parts and its main bioactive metabolites, Product Details of C17H18N2O6, the main research area is ethanol soluble tagetes lucida antihypertensive vasorelaxant mode bioactive metabolite; Antihypertensive; Calcium channel blockade; Coumarins; NO/cGMP system; Tagetes lucida; Vasorelaxant.

Tagetes lucida Cav. commonly known as “”yauhtli”” or “”pericoń”” is used in Mexican traditional medicine for the treatment of anxiety, depressant diseases, pain, hypertension, among others. To evaluate the antihypertensive and vasorelaxant modes of action of a crude ethanolic extract from T. lucida aerial parts and to isolate the bioactive compounds Ethanolic extract was tested in an in vivo assay in SHR rats by intragastric administration at 10 and 100 mg/kg dosages, to measure and to compare hemodynamic parameters like diastolic and systolic blood pressure and heart rate. Also, extract (3.03-1000μg/mL), fractions (3.03-1000μg/mL) and pure isolated compounds (1.75-550μM) were evaluated on isolated aortic rings contracted with noradrenaline (0.1μM) to determine their vasorelaxant effect and extract-mode of action.Ethanolic extract of T. lucida lowered systolic and diastolic blood pressure on SHR rats without heart rate modification (P > 0.05). Moreover, the extract showed concentration-dependent relaxant effect in a partially endothelium-dependent manner (P < 0.05), through NO/cGMP system activation and calcium channel blockade. 6,7,8-trimethoxycoumarin (1), 6,7-dimethoxycoumarin (2), and 7-methoxycoumarin (3) from T. lucida are the main bioactive compounds of the extract and showed significant vasorelaxant activity. Results provide evidence and endorsed the antihypertensive properties attributed to T. lucida in traditional medicine, which is produced by vasorelaxant effect mainly through multitarget NO/cGMP system activation and calcium channel blockade. Coumarin derivatives 1, 2 and 3 are the responsible of the vasorelaxant activity. Journal of Ethnopharmacology published new progress about Adrenoceptors Role: PAC (Pharmacological Activity), BIOL (Biological Study). 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

Choe, So-Hui published the artcileEffect of nifedipine, a calcium channel blocker, on the generation of nitric oxide and interleukin-1β by murine macrophages activated by lipopolysaccharide from Prevotella intermedia, Related Products of pyridine-derivatives, the main research area is calcium blockeron nitric oxide interleukin 1 beta lipopolysaccharide; Interleukin-1β; Lipopolysaccharide; Nifedipine; Nitric oxide; Periodontal disease.

The current study was undertaken to explore the influence of nifedipine on the generation of proinflammatory mediators by murine macrophages activated by lipopolysaccharide (LPS) prepared from Prevotella intermedia, a putative periodontal pathogen, and associated mechanisms of action as well. Real-time PCR and immunoblotting were conducted to quantify mRNA and protein expression, resp. NF-κB-dependent secreted embryonic alk. phosphatase (SEAP) levels were estimated by reporter assay. Nifedipine markedly suppressed the generation of iNOS-derived NO and IL-1β together with their mRNA expressions in murine macrophages activated by P. intermedia LPS. LPS-stimulated cells exposed to nifedipine notably increased the mRNA levels of Arg-1, Ym-1, FIZZ1, and TGF-β, which are typical markers for M2 macrophage polarization. Nifedipine induced HO-1 at both gene and protein levels in cells challenged with P. intermedia LPS, and the nifedipine-mediated inhibition of NO generation was significantly abrogated by adding SnPP, an HO-1 inhibitor. Nifedipine inhibited LPS-evoked generation of NO and IL-1β in a PPAR-γ-independent manner. Nifedipine is an inhibitor of P. intermedia LPS-evoked production of NO and IL-1β in murine macrophages and encourages macrophage polarization toward the M2 phenotype. Nifedipine possibly has potential to be used for host modulation of periodontal disease and is worth being further researched.

Naunyn-Schmiedeberg’s Archives of Pharmacology published new progress about Antigens, LyM-1 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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

Ghirardini, Elsa published the artcileMutant prion proteins increase calcium permeability of AMPA receptors, exacerbating excitotoxicity, Quality Control of 21829-25-4, the main research area is prion protein calcium AMPA receptor mutation excitotoxicity.

Prion protein (PrP) mutations are linked to genetic prion diseases, a class of phenotypically heterogeneous neurodegenerative disorders with invariably fatal outcome. How mutant PrP triggers neurodegeneration is not known. Synaptic dysfunction precedes neuronal loss but it is not clear whether, and through which mechanisms, disruption of synaptic activity ultimately leads to neuronal death. Here we show that mutant PrP impairs the secretory trafficking of AMPA receptors (AMPARs). Specifically, intracellular retention of the GluA2 subunit results in synaptic exposure of GluA2-lacking, calcium-permeable AMPARs, leading to increased calcium permeability and enhanced sensitivity to excitotoxic cell death. Mutant PrPs linked to different genetic prion diseases affect AMPAR trafficking and function in different ways. Our findings identify AMPARs as pathogenic targets in genetic prion diseases, and support the involvement of excitotoxicity in neurodegeneration. They also suggest a mechanistic explanation for how different mutant PrPs may cause distinct disease phenotypes.

PLoS Pathogens published new progress about AMPA receptors Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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, Quality Control of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Furini, Cristiane R. G. published the artcileMolecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is hippocampus memory synaptic protein BDNF; AMPA receptors; BDNF; CaMKII; L-VDCCs calcium channels; ORM consolidation; ORM reconsolidation.

Acquired information is stabilized into long-term memory through a process known as consolidation. Though, after consolidation, when stored information is retrieved they can susceptible, allowing modification, updating, strengthening and re-stabilized a new process referred to as memory reconsolidation. Also, considering that the study of link between synaptic proteins is key to understanding of memory processes, we investigated, in male Wistar rats, mol. mechanisms in the hippocampus involved on ORM consolidation and reconsolidation. We verified that the blockade of AMPAr and L-VDCCs calcium channels impaired ORM consolidation and reconsolidation when administered into CA1 immediately after sample phase or reactivation phase and that these impairments were blocked by the administration of AMPAr agonist and of neurotrophin BDNF. Also, the blockade of CaMKII impaired ORM consolidation when administered 3 h after sample phase but had no effect on ORM reconsolidation and its effect was blocked by the administration of BDNF, but not of AMPAr agonist. So, this study provides new evidence of the mol. mechanisms involved on the consolidation and reconsolidation of ORM, demonstrating that AMPAr and L-VDCCs are necessary for the consolidation and reconsolidation of ORM while CaMKII is necessary only for the consolidation and also that there is a link between BDNF and AMPAr, L-VDCCs and CaMKII as well as a link between AMPAr and L-VDCCs on ORM consolidation and reconsolidation.

Neuroscience (Amsterdam, Netherlands) published new progress about AMPA receptors Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Lang, Richard J. published the artcilePacemaker mechanisms driving pyeloureteric peristalsis: modulatory role of interstitial cells, HPLC of Formula: 21829-25-4, the main research area is review calcium cationic channel smooth muscle peristaltic pressure pacemaker; Atypical smooth muscle cells; Calcium channels; Calcium imaging; Interstitial cells; Pacemaking; Pyeloureteric peristalsis; Upper urinary tract.

The peristaltic pressure waves in the renal pelvis that propel urine expressed by the kidney into the ureter towards the bladder have long been considered to be ‘myogenic’, being little affected by blockers of nerve conduction or autonomic neurotransmission, but sustained by the intrinsic release of prostaglandins and sensory neurotransmitters. In uni-papilla mammals, the funnel-shaped renal pelvis consists of a lumen-forming urothelium and a stromal layer enveloped by a plexus of ‘typical’ smooth muscle cells (TSMCs), in multi-papillae kidneys a number of minor and major calyces fuse into a large renal pelvis. Electron microscopic, electrophysiol. and Ca2+ imaging studies have established that the pacemaker cells driving pyeloureteric peristalsis are likely to be morphol. distinct ‘atypical’ smooth muscle cells (ASMCs) that fire Ca2+ transients and spontaneous transient depolarizations (STDs) which trigger propagating nifedipine-sensitive action potentials and Ca2+ waves in the TSMC layer. In uni-calyceal kidneys, ASMCs predominately locate on the serosal surface of the proximal renal pelvis while in multi-papillae kidneys they locate within the sub-urothelial space. ‘Fibroblast-like’ interstitial cells (ICs) located in the sub-urothelial space or adventitia are a mixed population of cells, having regional and species-dependent expression of various Cl-, K+, Ca2+ and cationic channels. ICs display asynchronous Ca2+ transients that periodically synchronize into bursts that accelerate ASMC Ca2+ transient firing. This review presents current knowledge of the architecture of the proximal renal pelvis, the role Ca2+ plays in renal pelvis peristalsis and the mechanisms by which ICs may sustain/accelerate ASMC pacemaking.

Advances in Experimental Medicine and Biology published new progress about Prostaglandins Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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