Search results for: Charybdotoxin
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Diabetes modifies the role of prostanoids and potassium channels which regulate the hypereactivity of the rabbit renal artery to BNP.Diabetic nephropathy is associated with increased risk of cardiovascular disease. B-type natriuretic peptide (BNP) plays an important role in cardiovascular pathophysiology and therapeutics. The aim of the present study was to investigate the influence of experimental diabetes on the mechanisms that regulate the relaxant response of the rabbit renal artery to BNP. Arterial relaxations to BNP were enhanced in diabetic rabbits. Indomethacin enhanced BNP-induced relaxation in control rabbits but showed no effect in diabetic rabbits. BNP-induced release of thromboxane Aor prostacyclin was not different in both groups of animals. Iberiotoxin had no effect on relaxations to BNP in both groups of animals. Charybdotoxin displaced to the right the concentration-response curve to BNP in both group of animals, and inhibited BNP-induced relaxation only in diabetic rabbits. Glibenclamide did not modify the BNP-induced relaxations in control rabbits, but inhibited it in diabetic rabbits. These results suggest that diabetes induces hypereactivity of the rabbit renal artery to BNP by mechanisms that at least include (1) a reduced vasoconstrictor influence of arachidonic acid metabolites via cyclooxygenase 2, which is not related with changes in thromboxane Aand prostacyclin release from the arterial wall and (2) a selectively increased modulatory activity of Kand endothelial IKchannels.
1870 related Products with: Diabetes modifies the role of prostanoids and potassium channels which regulate the hypereactivity of the rabbit renal artery to BNP.TCP-1 theta antibody Sour Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit Anti-Theophylline FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Rabbit anti PKC theta (pS BACTERIOLOGY BACTEROIDES Recombinant Thermostable
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Hyperpolarization by N-(3-oxododecanoyl)-l-homoserine-lactone, a quorum sensing molecule, in rat thymic lymphocytes.To study the adverse effects of N-(3-oxododecanoyl)-l-homoserine-lactone (ODHL), a quorum sensing molecule, on mammalian host cells, its effect on membrane potential was examined in rat thymic lymphocytes using flow cytometric techniques with a voltage-sensitive fluorescent probe. As 3-300 μM ODHL elicited hyperpolarization, it is likely that it increases membrane Kpermeability because hyperpolarization is directly linked to changing Kgradient across membranes, but not Naand Clgradients. ODHL did not increase intracellular Caconcentration. ODHL also produced a response in the presence of an intracellular Znchelator. Thus, it is unlikely that intracellular Caand Znare attributed to the response. Quinine, a non-specific Kchannel blocker, greatly reduced hyperpolarization. However, because charybdotoxin, tetraethylammonium chloride, 4-aminopyridine, and glibenclamide did not affect it, it is pharmacologically hypothesized that Ca-activated Kchannels, voltage-gated Kchannels, and ATP-sensitive Kchannels are not involved in ODHL-induced hyperpolarization. Although the Kchannels responsible for ODHL-induced hyperpolarization have not been identified, it is suggested that ODHL can elicit hyperpolarization in mammalian host cells, disturbing cellular functions.
2902 related Products with: Hyperpolarization by N-(3-oxododecanoyl)-l-homoserine-lactone, a quorum sensing molecule, in rat thymic lymphocytes.Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki
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Important role of endothelium-dependent hyperpolarization in pulmonary microcirculation in male mice -Implications for hypoxia-induced pulmonary hypertension.Endothelium-dependent hyperpolarization (EDH) plays important roles in systemic circulation, whereas its role in pulmonary circulation remains largely unknown. Furthermore, the underlying mechanisms of pulmonary hypertension (PH) also remain to be elucidated. We thus aimed to elucidate the role of EDH in pulmonary circulation in general and in PH in particular. In isolated perfused lung using male wild-type mice, endothelium-dependent relaxations to bradykinin (BK) were significantly reduced in the presence of N-nitro-L-arginine (L-NNA) by ~50% as compared with those in the presence of indomethacin, and the combination of apamin plus charybdotoxin abolished the residual relaxations, showing the comparable contributions of nitric oxide (NO) and EDH in pulmonary microcirculation under physiological conditions. Catalase markedly inhibited EDH-mediated relaxations, indicating the predominant contribution of endothelium-derived hydrogen peroxide. BK-mediated relaxations were significantly reduced at day 1 of hypoxia, while thereafter remained unchanged until day 28. EDH-mediated relaxations were diminished at day 2 of hypoxia, indicating a transition from EDH to NO in BK-mediated relaxations prior to the development of hypoxia-induced PH. Mechanistically, chronic hypoxia enhanced eNOS expression and activity associated with downregulation of caveolin-1. Nitrotyrosine levels were significantly higher in vascular smooth muscle of pulmonary microvessels under chronic hypoxia than under normoxia. Similar transition of the mediators in BK-mediated relaxations was also noted in Sugen hypoxia mouse model. These results indicate that EDH plays important roles in pulmonary microcirculation in addition to NO under normoxic conditions and that impaired EDH-mediated relaxations and subsequent nitrosative stress may be potential triggers of the onset of PH.
2493 related Products with: Important role of endothelium-dependent hyperpolarization in pulmonary microcirculation in male mice -Implications for hypoxia-induced pulmonary hypertension.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Epstein-Barr Virus TGF beta induced factor 2 Tide Fluor™ 8 maleimide
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Beneficial effect of Berberis amurensis Rupr. on penile erection.To investigate whether the methanol extract of Berberis amurensis Rupr. (BAR) augments penile erection using in vitro and in vivo experiments.
Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein
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Inhibitory Effect of Interferons on Contractive Activity of Bovine Mesenteric Lymphatic Vessels and Nodes.We studied the effect of IFNα-2b and IFNβ-1a on phasic and tonic contractions of isolated bovine mesenteric lymphatic vessels and nodes. IFNα-2b and IFNβ-1a in concentrations of 250-1000 U/ml produced dose-dependent negative chronotropic and inotropic effects on spontaneous phasic contractions and tonus of lymphatic vessels and nodes. In de-endothelialized lymphatic vessels and nodes, IFNα-2b and IFNβ-1a in the same concentrations had less pronounced inhibitory effect on spontaneous contraction and tonus. L-NAME (100 μM) and charybdotoxin (0.1 μM with 0.5 μM apamine) significantly attenuated the inhibitory effect of IFNα-2b on phasic and tonic contractions of lymph nodes. L-NAME (100 μM) and indomethacin (10 μM) significantly reduced the IFNα-2b-induced inhibitory effect on phasic and tonic contractions of lymph node. These results indicate that IFNα-2b and IFNβ-1a have a pronounced inhibitory effect on the phasic and tonic contractions of bovine mesenteric lymphatic vessels and nodes. The responses are endothelium-dependent and are determined by production of NO and endothelium-dependent hyperpolarizing factor by endotheliocytes in lymphatic vessels and by production of NO and prostacyclin by endotheliocytes in the lymphatic nodes.
2365 related Products with: Inhibitory Effect of Interferons on Contractive Activity of Bovine Mesenteric Lymphatic Vessels and Nodes.Bovine Androstenedione,AS Ofloxacin CAS Number [824 Rapid Microplate Assay K Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl
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Low-Frequency Components in Rat Pial Arteriolar Rhythmic Diameter Changes.This study aimed to analyze the frequency components present in spontaneous rhythmic diameter changes in rat pial arterioles. Pial microcirculation was visualized by fluorescence microscopy. Rhythmic luminal variations were evaluated via computer-assisted methods. Spectral analysis was carried out on 30-min recordings under baseline conditions and after administration of acetylcholine (Ach), papaverine (Pap), Nω-nitro-L-arginine (L-NNA) prior to Ach, indomethacin (INDO), INDO prior to Ach, charybdotoxin and apamin, and charybdotoxin and apamin prior to Ach. Under baseline conditions all arteriolar orders showed 3 frequency components in the ranges of 0.0095-0.02, 0.02-0.06, and 0.06-0.2 Hz, another 2 in the ranges of 0.2-2.0 and 2.5-4.5 Hz, and another ultra-low-frequency component in the range of 0.001-0.0095 Hz. Ach caused a significant increase in the spectral density of the frequency components in the range of 0.001-0.2 Hz. Pap was able to slightly increase spectral density in the ranges of 0.001-0.0095 and 0.0095-0.02 Hz. L-NNA mainly attenuated arteriolar responses to Ach. INDO prior to Ach did not affect the endothelial response to Ach. Charybdotoxin and apamin, suggested as endothelium-derived hyperpolarizing factor inhibitors, reduced spectral density in the range of 0.001-0.0095 Hz before and after Ach administration. In conclusion, regulation of the blood flow distribution is due to several mechanisms, one of which is affected by charibdotoxin and apamin, modulating the vascular tone.
2693 related Products with: Low-Frequency Components in Rat Pial Arteriolar Rhythmic Diameter Changes.Sterile filtered rat ser Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Insulin 1 (Rat), syntheti Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN
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Vascular activation of Kchannels and Na-KATPase activity of estrogen-deficient female rats.The goal of the present study was to evaluate vascular potassium channels and Na-K-ATPase activity in estrogen deficient female rats. Female rats that underwent ovariectomy were assigned to receive daily treatment with placebo (OVX) or estrogen replacement (OVX+E2, 1mg/kg, once a week, i.m.). Aortic rings were used to examine the involvement of Kchannels and Na-K-ATPase in vascular reactivity. Acetylcholine (ACh)-induced relaxation was analyzed in the presence of L-NAME (100μM) and Kchannels blockers: tetraethylammonium (TEA, 5mM), 4-aminopyridine (4-AP, 5mM), iberiotoxin (IbTX, 30nM), apamin (0.5mM), charybdotoxin (ChTX, 0.1mM) and iberiotoxin plus apamin. When aortic rings were pre-contracted with KCl (60mM) or pre-incubated with TEA (5mM), 4-aminopyridine (4-AP, 5mM) and iberiotoxin (IbTX, 30nM) plus apamin (0.5μM), the ACh-induced relaxation was less effective in the ovariectomized group. Additionally, 4-AP and IbTX decreased the relaxation by sodium nitroprusside in all groups but this reduction was greater in the ovariectomized group. Estrogen deficiency also increased aortic functional Na-KATPase activity evaluated by K-induced relaxation. L-NAME or endothelium removal were not able to block the increase in aortic functional Na-KATPase activity, however, TEA (5mM) restored this increase to the control level. We also found that estrogen deficiency increased superoxide anion production and reduced nitric oxide release in aortic ring from ovariectomized animals. In summary, our results emphasize that the process underlying ACh-induced relaxation is preserved in ovariectomized animals due to the activation of Kchannels and increased Na-KATPase activity.
1484 related Products with: Vascular activation of Kchannels and Na-KATPase activity of estrogen-deficient female rats.Ofloxacin CAS Number [824 Rapid Microplate Assay K Estrogen Receptor; Clone Estrogen Receptor; Clone Estrogen Receptor; Clone Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Estrogen Receptor á (Pho Estrogen Receptor á (Pho Estrogen Receptor á (Pho Estrogen Receptor á (Pho
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Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats.Clobenzorex is a metabolic precursor of amphetamine indicated for the treatment of obesity. Amphetamines have been involved with cardiovascular side effects such as hypertension and pulmonary arterial hypertension. The aim of the present study was to investigate whether the direct application of 10-9-10-5 M clobenzorex on isolated phenylephrine-precontracted rat aortic rings produces vascular effects, and if so, what mechanisms may be involved. Clobenzorex produced an immediate concentration-dependent vasorelaxant effect at the higher concentrations (10-7.5-10-5 M). The present outcome was not modified by 10-6 M atropine (an antagonist of muscarinic acetylcholine receptors), 3.1×10-7 M glibenclamide (an ATP-sensitive K+ channel blocker), 10-3 M 4-aminopyridine (4-AP; a voltage-activated K+ channel blocker), 10-5 M indomethacin (a prostaglandin synthesis inhibitor), 10-5 M clotrimazole (a cytochrome P450 inhibitor) or 10-5 M cycloheximide (a general protein synthesis inhibitor). Contrarily, the clobenzorex-induced vasorelaxation was significantly attenuated (P<0.05) by 10-5 M L-NAME (a direct inhibitor of nitric oxide synthase), 10-7 M ODQ (an inhibitor of nitric oxide-sensitive guanylyl cyclase), 10-6 M KT 5823 (an inhibitor of protein kinase G), 10-2 M TEA (a Ca2+-activated K+ channel blocker and non-specific voltage-activated K+ channel blocker) and 10-7 M apamin plus 10-7 M charybdotoxin (blockers of small- and large-conductance Ca2+-activated K+ channels, respectively), and was blocked by 8×10-2 M potassium (a high concentration) and removal of the vascular endothelium. These results suggest that the direct vasorelaxant effect by clobenzorex on phenylephrine-precontracted rat aortic rings involved stimulation of the NO/cGMP/PKG/Ca2+-activated K+ channel pathway.
1683 related Products with: Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats.BYL-719 Mechanisms: PI3K- anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl GLP 2 ELISA Kit, Rat Prog Anti 3 DG imidazolone Mon ABT-263 Mechanisms: Bcl-2 ABT-737 Mechanisms: Bcl-2 AS-703026 Mechanisms: MEK AZD-6244 Mechanisms: MEK AZD-8055 Mechanisms: mTOR BEZ-235 Mechanisms: PI3K
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Altered neurobiological function of brainstem hypoglossal neurons in DiGeorge/22q11.2 Deletion Syndrome.DiGeorge/22q11.2 Deletion Syndrome (22q11DS) is a common genetic microdeletion syndrome that underlies several neurodevelopmental disorders including autism, attention deficit/hyperactivity disorder, and schizophrenia. In addition to cognitive impairments, those with 22q11DS have disrupted feeding and swallowing from birth onward. This perinatal dysphagia significantly compromises nutritional status, impairs appropriate weight gain, and can lead to life threatening aspiration-based infections. Appropriately timed excitation and inhibition of brainstem hypoglossal motor neurons, which innervate tongue muscles, is essential for proper feeding and swallowing. In this study we have examined changes in hypoglossal motor neuron function in the LgDel mouse model of 22q11DS. Hypoglossal motor neurons from LgDel mouse pups have action potentials with afterhyperpolarizations, mediated by a large conductance charybdotoxin-sensitive Ca-activated K current, that are significantly shorter in duration and greater in magnitude than those in wild-type pups. In addition, the amplitude, but not frequency, of glutamatergic excitatory glutamatergic postsynaptic currents (EPSCs) is diminished, and GABAergic, but not glycinergic, neurotransmission to hypoglossal motor neurons was reduced in LgDel animals. These observations provide a foundation for understanding the neurological changes in hypoglossal motor neuron function and their contribution to swallowing abnormalities that occur in DiGeorge/22q11.2 Deletion Syndrome.
1866 related Products with: Altered neurobiological function of brainstem hypoglossal neurons in DiGeorge/22q11.2 Deletion Syndrome.ING1B antisense ING1B sense Interferon γ p19 INK4D AKT1 (dn) Inducible Insulin Insulin promoter factor 1 Human Interleukin-7 IL-7 Human Macrophage Inflamma Human Macrophage Inflamma Human Interleukin-16 IL-1 Human Interleukin-33 IL-3
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Mechanism of resveratrol-induced relaxation in the human gallbladder.Resveratrol is a polyphenolic compound extracted from plants and is also a constituent of red wine. Resveratrol produces relaxation of vascular smooth muscle and may prevent cardiovascular diseases. Although resveratrol has been reported to cause relaxation of the guinea pig gallbladder, limited data are available about the effect of resveratrol on the gallbladder smooth muscle in humans. The purpose of this study was to investigate the relaxation effects of resveratrol in human gallbladder muscle strips.
Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Human Epstein-Barr Virus TGF beta induced factor 2 Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7 Human Interleukin-2 IL-2 Human Macrophage Inflamma
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