Relevant bibliographies by topics / EDHF

Academic literature on the topic 'EDHF'

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Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "EDHF"

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Hasunuma, K., T. Yamaguchi, D. M. Rodman, R. F. O'Brien, and I. F. McMurtry. "Effects of inhibitors of EDRF and EDHF on vasoreactivity of perfused rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 2 (February 1, 1991): L97—L104. http://dx.doi.org/10.1152/ajplung.1991.260.2.l97.

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Recent studies indicate that the endothelium of isolated rat pulmonary arteries releases two different factors, endothelium-derived relaxing factor (EDRF) and hyperpolarizing factor (EDHF), which participate in histamine- and acetylcholine-induced relaxation. There is evidence for EDRF vasoreactivity in perfused lungs, but a role for EDHF, which hyperpolarizes vascular smooth muscle by activating membrane K+ channels, has not been reported. We used the inhibitors of EDRF, 20 microM hemoglobin, 200 microM NG-mono-methyl-L-arginine, and 2 mM L-canavanine, the nonselective blocker of K+ channels, 10 mM tetraethylammonium (TEA), and the inhibitor of ATP-sensitive K+ channels, 20 microM glibenclamide, to compare the roles of EDRF and EDHF in the vasoregulation of meclofenamate-treated, salt solution-perfused rat lungs. The three EDRF inhibitors had little or no effect on baseline perfusion pressure, but each potentiated the peak pressor response to airway hypoxia. Neither of them inhibited the pulmonary vasodilation to 5 microM histamine. TEA, but not glibenclamide, increased baseline pressure and potentiated the peak hypoxic response. Both K+ channel blockers, but not the EDRF inhibitors, also prolonged the hypoxic response by reducing the rate of spontaneous vasodilation. TEA, but not glibenclamide, inhibited histamine vasodilation. These results suggest roles for both EDRF and EDHF in the control of rat pulmonary vascular reactivity. EDRF is apparently not responsible for the low vascular tone of the normoxic lung and does not mediate the vasodilation to histamine, but it does modulate the hypoxic pressor response. The exact role of EDHF is uncertain, but it may also modulate hypoxic vasoconstriction and mediate at least part of the histamine vasodilation.
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Park, Yoonjung, Stefano Capobianco, Xue Gao, John R. Falck, Kevin C. Dellsperger, and Cuihua Zhang. "Role of EDHF in type 2 diabetes-induced endothelial dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (November 2008): H1982—H1988. http://dx.doi.org/10.1152/ajpheart.01261.2007.

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Endothelium-derived hyperpolarizing factor (EDHF) plays a crucial role in modulating vasomotor tone, especially in microvessels when nitric oxide-dependent control is compromised such as in diabetes. Epoxyeicosatrienoic acids (EETs), potassium ions (K+), and hydrogen peroxide (H2O2) are proposed as EDHFs. However, the identity (or identities) of EDHF-dependent endothelial dilators has not been clearly elucidated in diabetes. We assessed the mechanisms of EDHF-induced vasodilation in wild-type (WT, normal), db/db (advanced type 2 diabetic) mice, and db/db mice null for TNF (dbTNF−/dbTNF−). In db/db mice, EDHF-induced vasodilation [ACh-induced vasodilation in the presence of NG-nitro-l-arginine methyl ester (l-NAME, 10 μmol/l) and prostaglandin synthase inhibitor indomethacin (Indo, 10 μmol/l)] was diminished after the administration of catalase (an enzyme that selectively dismutates H2O2 to water and oxygen, 1,000 U/ml); administration of the combination of charybdotoxin (a nonselective blocker of intermediate-conductance Ca2+-activated K+ channels, 10 μmol/l) and apamin (a selective blocker of small-conductance Ca2+-activated K+ channels, 50 μmol/l) also attenuated EDHF-induced vasodilation, but the inhibition of EETs synthesis [14,15-epoxyeicosa-5(Z)-enoic acid; 10 μmol/l] did not alter EDHF-induced vasodilation. In WT controls, EDHF-dependent vasodilation was significantly diminished after an inhibition of K+ channel, EETs synthesis, or H2O2 production. Our molecular results indicate that mRNA and protein expression of interleukin-6 (IL-6) were greater in db/db versus WT and dbTNF−/dbTNF− mice, but neutralizing antibody to IL-6 (anti-IL-6; 0.28 mg·ml−1·kg−1 ip for 3 days) attenuated IL-6 expression in db/db mice. The incubation of the microvessels with IL-6 (5 ng/ml) induced endothelial dysfunction in the presence of l-NAME and Indo in WT mice, but anti-IL-6 restored ACh-induced vasodilation in the presence of l-NAME and Indo in db/db mice. In dbTNF−/dbTNF− mice, EDHF-induced vasodilation was greater and comparable with controls, but IL-6 decreased EDHF-mediated vasodilation. Our results indicate that EDHF compensates for diminished NO-dependent dilation in IL-6-induced endothelial dysfunction by the activation of H2O2 or a K+ channel in type 2 diabetes.
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Wang, Xuemei, Greg Trottier, and Rodger Loutzenhiser. "Determinants of renal afferent arteriolar actions of bradykinin: evidence that multiple pathways mediate responses attributed to EDHF." American Journal of Physiology-Renal Physiology 285, no. 3 (September 2003): F540—F549. http://dx.doi.org/10.1152/ajprenal.00127.2003.

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The determinants of bradykinin (BK)-induced afferent arteriolar vasodilation were investigated in the in vitro perfused hydronephrotic rat kidney. BK elicited a concentration-dependent vasodilation of afferent arterioles that had been preconstricted with ANG II (0.1 nmol/l), but this dilation was transient in character. Pretreatment with the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester (100 μmol/l) and the cyclooxygenase inhibitor ibuprofen (10 μmol/l) did not prevent this dilation when tone was established by ANG II but fully blocked the response when tone was established by elevated extracellular KCl, which suggests roles for both NO and endothelium-derived hyperpolarizing factor (EDHF). We had previously shown that the EDHF-like response of the afferent arteriole evoked by ACh was fully abolished by a combination of charybdotoxin (ChTX;10 nmol/l) and apamin (AP; 1 μmol/l). However, in the current study, treatment with ChTX plus AP only reduced the EDHF-like component of the BK response from 98 ± 5 to 53 ± 6% dilation. Tetraethylammonium (TEA; 1 mmol/l), which had no effect on the EDHF-induced vasodilation associated with ACh, reduced the EDHF-like response to BK to 88 ± 3% dilation. However, the combination of TEA plus ChTX plus AP abolished the response (0.3 ± 1% dilation). Similarly, 17-octadecynoic acid (17-ODYA) did not prevent the dilation when it was administered alone (77 ± 9% dilation) but fully abolished the EDHF-like response when added in combination with ChTX plus AP (-0.5 ± 4% dilation). These findings suggest that BK acts via multiple EDHFs: one that is similar to that evoked by ACh in that it is blocked by ChTX plus AP, and a second that is blocked by either TEA or 17-ODYA. Our finding that a component of the BK response is sensitive to TEA and 17-ODYA is consistent with previous suggestions that the EDHF released by BK is an epoxyeicosatrienoic acid.
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Luksha, Leanid, Henry Nisell, Natallia Luksha, Marius Kublickas, Kjell Hultenby, and Karolina Kublickiene. "Endothelium-derived hyperpolarizing factor in preeclampsia: heterogeneous contribution, mechanisms, and morphological prerequisites." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R510—R519. http://dx.doi.org/10.1152/ajpregu.00458.2007.

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We hypothesized that in preeclampsia (PE), contribution of endothelium-derived hyperpolarizing factor (EDHF) and the mechanism/s of its action differ from that in normal pregnancy (NP). We aimed to assess endothelial function and morphology in arteries from NP and PE with particular focus on EDHF. Arteries (≈200 μm) were dissected from subcutaneous fat biopsies obtained from women undergoing cesarean section. With the use of wire myography, responses to the endothelium-dependent agonist bradykinin (BK) were determined before and after inhibition of pathways relevant to EDHF activity. The overall responses to BK in arteries from PE ( n = 13) and NP ( n = 17) were similar. However, in PE, EDHF-mediated relaxation was reduced ( P < 0.05). All women within the PE group were divided into two subgroups: with more ( group 1) or less ( group 2) than 50% reduction of EDHF-typed responses after 18-α-glycyrrhetinic acid (an inhibitor of myoendothelial gap junctions, MEGJs). The division showed that 1) MEGJs are principally involved when the EDHF contribution is reduced; and 2) when the EDHF contribution is similar to that in NP, the H2O2 and/or cytochrome P-450 epoxygenase products of arachidonic acid (AA), along with MEGJs, confer EDHF-mediated relaxation. In contrast, MEGJs were the main pathway for EDHF in NP. The abundant presence of MEGJs in arteries from NP but deficiency of them in PE was observed using transmission electron microscopy. We conclude that PE is associated with heterogeneous contribution of EDHF, and the mechanism behind EDHF-typed responses is mediated either by MEGJs alone or in combination with H2O2 or cytochrome P-450 epoxygenase metabolites of AA.
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Hayakawa, H., Y. Hirata, E. Suzuki, T. Sugimoto, H. Matsuoka, K. Kikuchi, T. Nagano, M. Hirobe, and T. Sugimoto. "Mechanisms for altered endothelium-dependent vasorelaxation in isolated kidneys from experimental hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (May 1, 1993): H1535—H1541. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1535.

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To study mechanisms for attenuated endothelium-dependent vasorelaxation in hypertension, we examined the effects of acetylcholine (ACh) on renal vascular resistance (RVR) and release rates of endothelium-derived relaxing factor (EDRF) in kidneys isolated from spontaneously hypertensive rats (SHR), deoxycorticosterone acetate (DOCA) salt-hypertensive (DOCA salt) rats, and Dahl salt-sensitive (Dahl S) rats. Decreases in RVR by ACh were smaller in hypertensive rats than in their normotensive controls. The release rate of nitric oxide into the perfusate, which was estimated using nitrite-nitrate as an index, did not differ between SHR and Wistar-Kyoto rats (WKY). However, the release rate of EDRF was markedly decreased in both DOCA salt rats and Dahl S rats compared with their normotensive controls (10(-7) M ACh: DOCA salt 45 +/- 6 vs. control 410 +/- 60 pmol.min-1.g-1 kidney wt, P < 0.001). In SHR, high-K+ perfusion or pretreatment with glibenclamide, inhibitors of endothelium-derived hyperpolarizing factor (EDHF), significantly reduced ACh-induced vasorelaxation only in WKY, resulting in no differences in the RVR reduction between SHR and WKY. Thus attenuated ACh-induced vasorelaxation in the SHR kidney may be attributed to a decrease in EDHF, but to a decrease in EDRF in DOCA salt rats and Dahl S rats.
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You, Junping, Elke M. Golding, and Robert M. Bryan. "Arachidonic acid metabolites, hydrogen peroxide, and EDHF in cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H1077—H1083. http://dx.doi.org/10.1152/ajpheart.01046.2004.

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We tested the hypotheses that EDHF in rat middle cerebral arteries (MCAs) involves 1) metabolism of arachidonic acid through the epoxygenase pathway, 2) metabolism of arachidonic acid through the lipoxygenase pathway, or 3) reactive oxygen species. EDHF-mediated dilations were elicited in isolated and pressurized rat MCAs by activation of endothelial P2Y2 receptors with either UTP or ATP. All studies were conducted after the inhibition of nitric oxide synthase and cyclooxygenase with Nω-nitro-l-arginine methyl ester (10 μM) and indomethacin (10 μM), respectively. The inhibition of epoxygenase with miconazole (30 μM) did not alter EDHF dilations to UTP, whereas the structurally different epoxygenase inhibitor N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanoic acid (20 or 40 μM) only modestly inhibited EDHF at the highest concentration of UTP. An antagonist of epoxyeicosatrienoic acids, 14,15-epoxyeicosa-5( Z)-enoic acid, had no effect on EDHF dilations to UTP. Chronic inhibition of epoxygenase in the rat with 1-aminobenzotriazol (50 mg/kg twice daily for 5 days) did not alter EDHF dilations. The inhibition of the lipoxygenase pathway with either 10 μM baicalein or 10 μM nordihydroguaiaretic acid produced no major inhibitory effects on EDHF dilations. The combination of superoxide dismutase (200 U/ml) and catalase (140 U/ml) had no effect on EDHF dilations. Neither tiron (10 mM), a cell-permeable scavenger of reactive oxygen species, nor deferoxamine (1 or 10 mM), an iron chelator that blocks the formation of hydroxyl radicals, altered EDHF dilations in rat MCAs. We conclude that EDHF dilations in the rat MCA do not involve the epoxygenase pathway, lipoxygenase pathway, or reactive oxygen species including H2O2.
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You, Junping, Sean P. Marrelli, and Robert M. Bryan. "Role of Cytoplasmic Phospholipase A2 in Endothelium-Derived Hyperpolarizing Factor Dilations of Rat Middle Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 22, no. 10 (October 2002): 1239–47. http://dx.doi.org/10.1097/01.wcb.0000037996.34930.2e.

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Very little is known regarding the mechanism of action for the endothelium-derived hyperpolarizing factor (EDHF) response in cerebral vessels. The authors tested two hypotheses: (1) activation of the cytoplasmic form of phospholipase A2 (cPLA2) is involved with EDHF-mediated dilations in rat middle cerebral arteries; and (2) activation of the cPLA2 involves an increase in endothelial Ca2+ through activation of phospholipase C. Middle cerebral arteries were isolated from the rat, pressurized to 85 mm Hg, and luminally perfused. The EDHF response was elicited by luminal application of uridine triphosphate (UTP) after NO synthase and cyclooxygenase inhibition (10−5 mol/L N-nitro-l-arginine methyl ester and 10−5 mol/L indomethacin, respectively). AACOCF3 and PACOCF3, inhibitors of cPLA2 (Ca2+-sensitive) and Ca2+-insensitive PLA2 (iPLA2), dose dependently attenuated the EDHF response. A selective inhibitor for iPLA2, haloenol lactone suicide substrate, had no effect on the EDHF response. The EDHF response elicited by UTP was accompanied by an increase in endothelial Ca2+ (144 to 468 nmol/L), and the EDHF dilation was attenuated with U73122, a phospholipase C inhibitor. The authors conclude that the EDHF response elicited by luminal UTP in rat middle cerebral arteries involved activation of phospholipase C, an increase in endothelial Ca2+, and activation of cPLA2.
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Chilian, William M., and Ryoji Koshida. "EDHF and NO." Circulation Research 89, no. 8 (October 12, 2001): 648–49. http://dx.doi.org/10.1161/res.89.8.648.

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Félétou, Michel, and Paul M. Vanhoutte. "EDHF: an update." Clinical Science 117, no. 4 (July 16, 2009): 139–55. http://dx.doi.org/10.1042/cs20090096.

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The endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term ‘endothelium-derived hyperpolarizing factor’ (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H2O2, CO, H2S and various peptides can be released by endothelial cells. These factors activate different families of K+ channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells, followed by the opening of SKCa and IKCa channels (small and intermediate conductance Ca2+-activated K+ channels respectively). These channels have a distinct subcellular distribution: SKCa are widely distributed over the plasma membrane, whereas IKCa are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SKCa activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IKCa activation, K+ efflux can activate smooth muscle Kir2.1 and/or Na+/K+-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases.
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Félétou, Michel, and Paul M. Vanhoutte. "The Alternative: EDHF." Journal of Molecular and Cellular Cardiology 31, no. 1 (January 1999): 15–22. http://dx.doi.org/10.1006/jmcc.1998.0840.

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Dissertations / Theses on the topic "EDHF"

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Höpfl, Bernd. "EDHF initiiert fortgeleitete Gefäßdilatationen in Arteriolen des Skelettmuskels." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-31718.

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Schach, Christian Oliver. "Mechanismus der EDHF-vermittelten Gefässdilatation der Arteria Interlobaris Suis /." Frankfurt a.M, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254594.

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Burnette, Ethan Williams. "Endothelium-derived hyperpolarizing factor (EDHF) in rat mesenteric artery." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66130.pdf.

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Charisis, Ioannis. "Role of calcium-dependent potassium channels and mitochondria in the EDHF phenomenon." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55773/.

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Background Acetylcholine (ACh) and the calcium ionophore A23187 are both known to trigger EDHF-type responses in the rabbit iliac artery via endothelial cell hyperpolarization mediated by the opening of calcium-dependent potassium channels (Kca). In addition, ACh and A23187 also stimulate the release of hydrogen peroxide (H2O2) from the endothelium. Aims of study 1) To determine the relative contribution of different Kca channel subtypes to ACh- and A23187-evoked responses. 2) To determine whether there is a connection between the activation of endothelial Kca channels and the release of H2O2. 3) To identify the source of endothelium-derived H2O2 in the rabbit iliac artery. Major findings 1) Immimohistochemical investigations demonstrated expression of SKca, IKca and BKca channels in the endothelium of rabbit iliac arteries. 2) Mechanical studies with the SKca inhibitor apamin, the IKca inhibitor l- (2- chlorophenyl)diphenylmethyl -lH-pyrazole (TRAM-34) and the BKca inhibitor iberiotoxin demonstrated that all three Kca channel subtypes participate in ACh- and A23187-evoked EDHF-type relaxations. 3) Mechanical investigations with catalase and the catalase/SOD-mimetic manganese porphyrin (MnTMPyP) demonstrated that responses to ACh and A23187 both included a significant H2C>2-dependent component, that could be inhibited by combined Kca channel blockade. 4) Investigations with the NADPH oxidase inhibitor apocynin, the xanthine oxidase inhibitor oxypurinol and the inhibitors of the mitochondrial electron transport chain rotenone and myxothiazol indicated that mitochondria are likely to be the main source of H2O2 in the endothelium of the rabbit iliac artery. Conclusions The study has highlighted the concerted role of different Kca channel subtypes in ACh- and A23187-evoked EDHF-type relaxations in rabbit iliac arteries. It has also demonstrated that both responses consist of an H202-dependent component which is attenuated when Kca channels are inhibited. However, the evidence provided is not sufficient to prove that H2O2 release in the endothelium is coupled to Kca activation Additional studies aimed to identify the intracellular compartment that produces H2O2 upon stimulation with ACh and A23187. It has been demonstrated that under the current experimental conditions the most likely source of H2O2 is the mitochondrial electron transport chain.
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Harris, David. "Pharmacological studies on EDHF and anandamide in the rat mesenteric arterial bed." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366599.

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Chauhan, Sharmila Deepa. "Mechanisms of endothelium-dependant dilation : a study of EDHF and endothelial dysfunction." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397184.

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Mather, Simon. "Endothelial cell modulation of vascular tone by EDHF and gap junctional communication." Thesis, University of Bath, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418594.

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Young, Elisa, and elisayoung@iprimus com au. "Endothelial dysfunction in insulin resistance: The role of EDHF and gap junction communication." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080110.162249.

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Background: Endothelial dysfunction is a key factor in the development of vascular complications in insulin resistance and diabetes and recent studies have established that endothelium-derived hyperpolarising factor (EDHF) plays an important physiological role in endothelium-derived relaxation responses, especially in small arteries and arterioles. Objective: This project aimed to identify the role of, and characterise, EDHF in animal models of insulin resistance, including the obese Zucker rat (OZR) as well as the fructose-fed (FF) Sprague-Dawley rat. Methods: Vascular function was studied in third-order mesenteric arteries from male and female Zucker rats using pressure myography, and in lobar arteries from male FF rats using wire myography. Endothelial function was determined by studying responses to the endothelium-dependent dilator acetylcholine (ACh) and the endothelium-independent dilator levcromakalim in the presence of a variety of inhibitors to study the roles of NO, EDHF and gap junctions. The effect of insulin resistance on gap junctions was further assessed by measuring the protein and mRNA expression of vascular connexins. Protein levels were determined by western blotting followed by semi-quantitative analysis of band intensity, whilst mRNA levels were quantified using real-time PCR, in which beta-actin was used as the housekeeping gene. Results: Metabolic parameter comparisons confirmed that male OZRs were type 2 diabetic, whilst female OZRs were insulin resistant. Responses to ACh were reduced in both the male and female OZRs compared with their gender controls, with the male OZR showing a greater degree of endothelial dysfunction. In all Zucker third-order mesenteric arteries, inhibition of NO had no effect; however inhibitors of EDHF abolished relaxation responses to ACh. Inhibitors of gap junctions associated with connexin 40 significantly (p less than 0.05, Student's t-test) attenuated the maximal response to ACh in the LZR, but had no effect in the OZR. Comparison of Western blot band intensity indicated that connexin 40 protein levels in mesenteric vascular homogenates in the OZR were significantly smaller (p less than 0.05, Student's t-test) than in the LZR, with no difference in connexin 43 protein levels. mRNA levels showed a significant (p less than 0.05, Student's t-test) decrease in connexin 40 expression in the OZR compar ed with the LZR, with no change in connexin 43 mRNA expression. Although FF rats did develop insulin resistance, responses to ACh were not altered in the FF rats as compared with their controls, and ACh responses were abolished by NO inhibitors. Conclusion: The findings presented in this thesis demonstrate that endothelial dysfunction is present in third-order mesenteric arteries from insulin-resistant female and type 2 diabetic male OZRs, and is associated with a defect in EDHF. However, endothelial function was not compromised in the insulin-resistant FF rats. Furthermore, the reduction in EDHF-mediated vasodilatation in the mesenteric arteries from female OZRs was associated with the functional absence of connexin 40-related gap junctions as well as a reduction in connexin 40 protein and mRNA levels. This novel finding suggests that gap junctions associated with connexin 40 may be a potential therapeutic target for diabetic vascular disease.
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Neininger, Michael. "Zelluläre Mechanismen der Dilatation isolierter Widerstandsarterien durch NO-Donatoren und den Endothelabhängigen Hyperpolarisierenden Faktor EDHF." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-27038.

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Riexinger, Tobias. "Ein Cytochrom P450 2C8/9-abhängig gebildeter EDHF hyperpolarisiert Thrombozyten und hemmt deren Adhäsion an Endothelzellen." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-89394.

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Books on the topic "EDHF"

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Feletou, Michel. EDHF: The complete story. Boca Raton, FL: CRC/Taylor & Francis, 2006.

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Aic, Aʻvān Ke. Edhi. 2nd ed. Karachi: Mehran Press International, 1987.

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Ymeri, Hysen. Stërvitëm edhe Adem Jasharin. Tiranë: Emal, 2009.

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Pëllumbi, Servet. Edhe politika do moral. Tiranë: Rinia & ISPS, 2005.

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Ndreko, Merita. "--edhe gjysma e Botës". Tiranë: Shtëpia Botuese "Dora d'Istria", 2005.

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Kraja, Mehmet. Edhe të çmendurit fluturojnë: Roman. Tiranë: Onufri, 2004.

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Kraja, Mehmet. Edhe të çmendurit fluturojnë: Roman. Tiranë: Onufri, 2012.

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Benzo, Raúl. El umbral de Edaf: Cuentos. Montevideo: Ediciones de la Banda Oriental, 1990.

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Dashi, Kujtim. Edhe një gotë Filipit: Tregime. Tiranë: Botimet Toena, 1998.

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Beqja, Hamit. Edhe engjëlli edhe djalli janë brenda te i gjalli: Rreth dyzimit të personalitetit njerëzor. Tiranë: Albinform, 1995.

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Book chapters on the topic "EDHF"

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"References." In EDHF, 177–277. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.bmatt.

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"The Blood Vessel Wall." In EDHF, 1–38. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch1.

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"Endothelium-Derived Mediators." In EDHF, 39–53. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch2.

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"Endothelium-Dependent Hyperpolarizations." In EDHF, 55–132. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch3.

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"EDHF and Endothelial Dysfunction." In EDHF, 145–60. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch5.

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"EDHF and Therapeutic Interventions." In EDHF, 161–72. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch6.

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"Conclusions." In EDHF, 173–75. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch7.

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"EDHF and the Physiological Control of Blood Flow." In EDHF, 133–44. CRC Press, 2005. http://dx.doi.org/10.1201/9781420023312.ch4.

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"Endothelium and smooth muscle pathways for conduction along resistance microvessels." In Edhf 2000, 50–59. CRC Press, 2003. http://dx.doi.org/10.1201/b12802-10.

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"Membrane potential and calcium responses evoked by acetylcholine in submucosal arterioles of the guinea-pig small intestine." In Edhf 2000, 60–68. CRC Press, 2003. http://dx.doi.org/10.1201/b12802-11.

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Conference papers on the topic "EDHF"

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Orie, Nelson, Aysha Bakhamis, Moataz Bashah, Mohammed Alsayrafi, and Vidya Mohamed Ali. "EDHF Contribution To Microvascular Dilatation Is Not Linked To Endothelial Dysfunction In Morbidly Obese Qataris." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0360.

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Lau, Rachel Y. W., and Hilary J. Kahn. "Information modelling of EDIF." In the 30th international. New York, New York, USA: ACM Press, 1993. http://dx.doi.org/10.1145/157485.164892.

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Griffith, T. M., D. H. Edwards, R. L. Davies, T. J. Harrison, and K. L. Evans. "EDRF AND RESISTANCE VESSELS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643721.

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The influence of endothelium on vasomotionin resistance vessels was studied in an isolated, buffer-perfused rabbit ear preparation using novel microangiographic techniques and haemoglobin as a specific inhibitor of EDRF. In constricted preparations acetylcholine and Substance P, whose action is EDRF-dependent in large vessels, induceddilatation in vessels down to 25um in diameter which was inhibited by haemoglobin. Log (IC50>q) values calculated from diameter changes were the same in the central artery, GO, and its first three generations of branch vessels Gl, G2 and G3 (ie down to 7Oum) being -7.7 and -9.8 respectively. Consistent with this, almost identical valueswere derived from the pressure responses of the intact network. Such spatial homogeneity has not been found when the same vessels are studied in isolation. In contrast,constrictor responses to 5HT or histamine exhibited spatial heterogeneity (in the rank order G0>G1>G2>G3) which was exaggerated by inhibition of basal EDRF activity. Inerms of normalised diameter changes EDRF and its analogue GTN were equipotent in reversing these constrictor responses in GO to G3. Interms of hydraulic resistance however, dilator responses paralleled relative changesn resistance induced by the constrictor agents. EDRF and GTN thus appear more potentin vessels exhibiting high degrees of tone.In control preparations (i.e. in the absence of pharmacological constriction) basal EDRF activity was found to exert maximal influence in vessels in which calculatedshear stress and hydraulic resistance werehighest, and continuously inhibited myogenic tope in Gl and to a lesser extent G2 and G3. In the absence of haemoglobin, diameter and flow were related by the expression QÒaD4+b in GO, Gl and G2 over an 8-fold range of flow rates. In the high-flow limit this implies constancyof pressure gradient and pressure drop inthese vessels so that the energy expended in delivering a given volume of perfusate to the terminal elements of the bed would be effectively independent of flow rate, rather than directly proportional to it as in a rigid tube.Basal EDRF activity also conferred identical flow-related distensibility in G0 through G3 in control and partially constricted preparations over the samerange of flow rates. This implies independence of flow distribution from flowrate. Flow dependent release of EDRF may provide a mechanism which links network topography with vessel function, thus optimising perfusion characteristics.
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Patterson, Jesse, and Thidapat Chantem. "EDF-hv." In RTNS '16: 24th International Conference on Real-Time Networks and Systems. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2997465.2997491.

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Huang, Benxiong, Fan Zhang, Yan Wang, and Xiaoling Wang. "IEEE 802.11e EDCF performance evaluation." In Asia-Pacific Optical and Wireless Communications, edited by Chih-Lin I, Jiann-An Tsai, and Hequan Wu. SPIE, 2004. http://dx.doi.org/10.1117/12.520233.

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Bardou-Jacquet, Antoine. "EDF la vallée." In the 29th International Conference. New York, New York, USA: ACM Press, 2002. http://dx.doi.org/10.1145/2931127.2931211.

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Roberts, M. "CEDIF: a data driven EDIF reader." In the 1989 26th ACM/IEEE conference. New York, New York, USA: ACM Press, 1989. http://dx.doi.org/10.1145/74382.74538.

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Shahdad, M. "An interface between VHDL and EDIF." In 24th ACM/IEEE conference proceedings. New York, New York, USA: ACM Press, 1987. http://dx.doi.org/10.1145/37888.37958.

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Shahdad, M. "An interface between VHDL and EDIF." In COMPCON Spring 88. IEEE, 1988. http://dx.doi.org/10.1109/cmpcon.1988.4881.

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Eurich, J. P. "EDIF: test generation and fault simulation." In COMPCON Spring 88. IEEE, 1988. http://dx.doi.org/10.1109/cmpcon.1988.4887.

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Reports on the topic "EDHF"

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Bui, Dai. Revision of a Non-Preemptive EDF Packet Scheduling Algorithm. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada538864.

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Teixeira, Joao. Unified Cloud and Mixing Parameterizations of the Marine Boundary Layer: EDMF and PDF-Based Cloud Approaches. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada598085.

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Teixeira, Joao. Unified Cloud and Mixing Parameterizations of the Marine Boundary Layer: EDMF and PDF-based Cloud Approaches. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada574017.

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Teixeira, Joao. Collaborative Project: An Integrated Parameterization of Boundary Layer and Convective Mixing: The Eddy-Diffusivity/Mass-Flux (EDMF) Approach. Office of Scientific and Technical Information (OSTI), June 2019. http://dx.doi.org/10.2172/1529045.

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Burchell, Timothy D. Experimental Plan for EDF Energy Creep Rabbit Graphite Irradiations- Rev. 2 (replaces Rev. 0 ORNL/TM/2013/49). Office of Scientific and Technical Information (OSTI), July 2014. http://dx.doi.org/10.2172/1143548.

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Emmitt, George D., Ralph Foster, and Stephan de Wekker. Investigation of the Representation of OLEs and Terrain Effects Within the Costal Zone in the EDMF Parameterization Scheme: An Airborne Doppler Wind Lidar Perspective. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612728.

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Emmitt, George D., Ralph Foster, Stephan De Wekker, and Steven Greco. Investigation of the Representation of OLEs and Terrain Effects Within the Coastal Zone in the EDMF Parameterization Scheme: An Airborne Doppler Wind Lidar Perspective. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada564621.

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Emmitt, George D., Ralph Foster, and Stephen de Wekker. Investigation of the Representation of OLEs and Terrain Effects Within the Coastal Zone in the EDMF Parameterization Scheme: An Airborne Doppler Wind Lidar Perspective. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada590709.

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Emmitt, George D., Ralph Foster, and Stephan De Wekker. Investigation of the Representation of OLEs and Terrain Effects within the Coastal Zone in the EDMF Parameterization Scheme: An Airborne Doppler Wind Lidar Perspective. Fort Belvoir, VA: Defense Technical Information Center, October 2015. http://dx.doi.org/10.21236/ada627183.

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Comerford, Milo, and Simeon Dukic. Ekstremizmi Online: Sfidat dhe Mundësitë në Ballkanin Perëndimor. RESOLVE Network, February 2021. http://dx.doi.org/10.37805/pn2021.7.wb.

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Ballkani Perëndimor përballet me një sfidë të dyfishtë si pasojë e ekstremizmit online. Platformat online po lehtësojnë shënjestrimin specifik të rajonit nga narrativa të ndryshme ekstremiste ndërkombëtare. Ndërkohë, historia dhe gjeopolitika rajonale po përvetësohen për të justifikuar veprimet dhe narrativat ekstremiste në mbarë botën. Sidoqoftë, ky fenomen është pjesë e një tendence më të gjerë, e cila vë në dukje sfidën gjithnjë e më të madhe që paraqet përhapja e ideologjive ekstremiste transkombëtare në platformat online, si ato xhihadiste të dhunshme ashtu edhe ato të ekstremit të djathtë. Në Ballkanin Perëndimor, kjo paraqet një sërë rreziqesh specifike.
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