جستجوی مقالات مرتبط با کلیدواژه « کانال پتاسیم » در نشریات گروه « پزشکی »

Rough endoplasmic reticulum is important organelle that plays a role in the regulation of a range of functions. Potassium channels in the endoplasmic reticulum membrane were recently reported that its physiological role is unknown. Hepatocyte endoplasmic reticulum is a rich source of glucose 6- phosphatase that is involved in the control of gluconeogenesis. Since phosphate ions are intra-luminal metabolites for this enzyme of endoplasmic reticulum thus, in this study, the effect of phosphate ions on potassium channel activity was studied. Endoplasmic reticulum vesicles extraction was accomplished following liver excision in rats, homogenization and several stages of ultracentrifugation. Phosphatidylcholine was extracted from fresh egg yolk. Bilayer lipid membrane was formed in a 350 µm diameter aperture in between two chambers cis and trans contained 200/50 mMKCl solutions respectively, then vesicles were incorporated into bilayer lipid membrane. Ion channel activity was recorded by single channel recording technique both in control conditions and presence of phosphate ion in luminal face, next biophysical ion channel properties analyzed by Clampfit10 software. Endoplasmic reticulum Potassium channel was 550 pS conductance and its activity changed as voltage dependent manner in voltage range of +30 to -40 mV, in this respect the open probability and the average unitary current in a voltage + 30 mV were 0.73 and 26 pA, respectively. However, at lower voltages, the channel activity was minimal. In the presence of 50 mM phosphate ion, mean unitary current and also channel open probability did not change significantly in different voltages compared to the control condition (p>0.05). Rat hepatocyte endoplasmic reticulum membranes has been a kind of potassium channel with voltage-dependent activity and it seems that its electrophysiological characteristics did not influenced by phosphate anion in luminal face.

It is generally accepted that the selective adenosine triphosphate-dependent potassium channel openers (KATP openers) have a dramatic role in the treatment of some cardiovascular disorders. The aim of this study was to investigate the effects of diazoxide, a potent ATP-related potassium channel opener, on spontaneously beating isolated rat atria to achieve more accurate approaches to treat cardiovascular diseases, such as atrial related disorders including atrial arrhythmias.

After induction of anesthesia, we exsected the heart and isolated the atria of 48 male Wistar rats. Later, we recorded the beating and contractile force of the atria by a physiograph. Subsequently, we studied the effects of diazoxide (2 to 100 µg/mL) on beating and contractile force of the isolated atria 5, 10, 15 and 20 minutes after applying the drug onto the atria.

Diazoxide administration (2 to 100 µg/mL) showed a significant decrease (7% to 49% depending on concentration) in atrial beatings (P≤0.001) and in contractile force (1.5% to 67% depending on concentration), (P≤0.001). The effects began several minutes after applying the drug onto the tissues.

This study revealed that diazoxide has a direct concentration-dependent effect on cardiac performance and leads to reduction in beating rates and contractile force of the heart. This effect seems to be related to the activation of mitochondrial or sarcolemmal KATP channels. Since the inhibitory action of diazoxide on the heart was very remarkable and prompt, this agent may also exhibit antiarrhythmic properties.

The G to A mutation in KCNJ11; the ATP-sensitive potassium channel subunit, results in glutamate (E) to lysine (K) substitution at codon 23, and the A allele is shown to have a relationship with type II diabetes in our previous study. Their role in coronary heart disease (CHD) is not exactly obvious. We hypothesized that the polymorphism would be associated with increased susceptibility to CHD. The E23K gene polymorphism of KCNJ11 gene was analyzed by PCR-restriction fragment length polymorphism (PCR-RFLP) methods in 55 controls and 73CHD patients. Serum lipids and Fasting Blood Sugar concentrations were measured in all subjects. Among the CHD patients, the frequency of the A allele was higher (34.9% vs. 26.4%, P<0.05) and the frequency of the G allele was lower (65.1% vs. 73.6%, P>0.05) than among controls. No significant differences were found in allele frequencies between CHD and controls (P>0.05). Also, there were no significant differences in GG and combined (GA+AA) genotypes frequencies (42.5% vs. 56.4%, and 57.5% vs. 43.6%, P>0.05). The E23K gene polymorphism in KCNJ11 gene has no association with the high susceptibility to CHD.

Multiple sclerosis (MS) is considered as a common inflammatory disease of the human central nervous system (CNS). 4 amino pyridine (4-AP), a potassium channel blocker, is used widely in MS treatment to reduce fatigue and cachexia often experienced by the patients. The objective of this study was to get a better understanding of the mechanism of action of this drug, using the cell culture model. More specifically, we attempted to determine the effects of the drug on 1. The profileration of, and its cytotoxicity on, the neurons, and 2. The activity of MMP-9 in the neurons.

Considering the available reports on the wide range of 4-AP effects, we designed this study to investigate its possible role in proliferation or cytotoxicity of the MS cellular model, i.e. astrocytoma U373-MG, using the MTT assay technique. We also analyzed the effect of 4-AP on cell functionality as assessed by matrix metalloproteinase-9 (MMP-9) zymography.

The results showed that while 4-AP at a concentration of 0.1 and 1 mM has no significant cytotoxic effects on the treated cells, it has remarkable MMP-9 inhibitory effects (p<0.01). The proliferation analyses confirmed the stability of 4-AP effects on cell functionality.

On the whole, the results of the present study show the desirable effect of 4-AP on MMP-9 activity at non-cytotoxic doses, promising its further therapeutic applications.

The vasorelaxant effect of estrogens on blood vessels is one of the important cardiovascular protective mechanisms of estrogen. The present experiments were designed to study the mechanisms of vasorelaxant effect of 17β-estradiol (E2) in human saphenous veins (HSV). HSV were obtained from patients undergoing coronary artery bypass graft surgery in Tabriz Madani Heart Center. The role of K+ channels and endothelium derived hyperpolarizing factor (EDHF) in the effects of E2 were studied by incubating tissues with K+ channels blockers: glibenclamid (3μM), 4-aminopyridin (1mm), tetraethyl ammonium (TEA, at lower and higher concentration: 1mm and 10mM), BaCl2 (30μM) and combination of charybdotoxin and apamin. In order to assess the role of endothelium in the inhibitory effect of TEA (10mM) on the relaxant effect of E2, responses were elicited in endothelium denuded vein rings. TEA at 1mm, (selective inhibitor of large-conductance, BKCa, Ca2+ activated K+ channels), 4- aminopyridin (selective inhibitor of voltage dependent K+ channels) and glibenclamid (selective inhibitor of ATP dependent K+ channels) did not affect the vasorelaxant effects of E2 on PGF2α-induced contractions. TEA at higher concentration, an inhibitor of small-conductance (SKCa) and intermediate-conductance (IKCa) Ca2+ activated K+ channels, significantly inhibited E2-induced vasorelaxation. This inhibitory effect was endothelium-dependent and abolished by endothelium denuding. In intact tissues, pretreatment either with a combination of charybdotoxin and apamin (inhibitors of EDHF), or BaCl2, significantly reduced the relaxation produced by E2. The data suggest that vasorelaxant effect of E2 in HSV maybe mediated by EDHF which involves apamin/charybdotoxin-sensitive K+-channels and K+.