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Journal articles on the topic 'EDHF'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

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,

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2

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 d

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3

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

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4

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 overa

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5

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 a

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6

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

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7

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 tr

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8

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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9

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 vas

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10

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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11

Parkington, Helena C., Marianne Tare, and Harold A. Coleman. "The EDHF Story." Circulation Research 102, no. 10 (May 23, 2008): 1148–50. http://dx.doi.org/10.1161/circresaha.108.177279.

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12

Takaki, Aya, Keiko Morikawa, Masato Tsutsui, Yoshinori Murayama, Ender Tekes, Hiroto Yamagishi, Junko Ohashi, Toyotaka Yada, Nobuyuki Yanagihara, and Hiroaki Shimokawa. "Crucial role of nitric oxide synthases system in endothelium-dependent hyperpolarization in mice." Journal of Experimental Medicine 205, no. 9 (August 11, 2008): 2053–63. http://dx.doi.org/10.1084/jem.20080106.

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The endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several relaxing factors, such as prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF). We have previously demonstrated in animals and humans that endothelium-derived hydrogen peroxide (H2O2) is an EDHF that is produced in part by endothelial NO synthase (eNOS). In this study, we show that genetic disruption of all three NOS isoforms (neuronal [nNOS], inducible [iNOS], and endothelial [eNOS]) abolishes EDHF responses in mice. The contribution of the NOS sy

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13

Morio, Yoshiteru, Ethan P. Carter, Masahiko Oka, and Ivan F. McMurtry. "EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 5 (May 1, 2003): H1762—H1770. http://dx.doi.org/10.1152/ajpheart.00831.2002.

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The role of endothelium-derived hyperpolarizing factor (EDHF) in regulating the pulmonary circulation and the participation of cytochrome P-450 (CYP450) activity and gap junction intercellular communication in EDHF-mediated pulmonary vasodilation are unclear. We tested whether tonic EDHF activity regulated pulmonary vascular tone and examined the mechanism of EDHF-mediated pulmonary vasodilation induced by thapsigargin in salt solution-perfused normotensive and hypoxia-induced hypertensive rat lungs. After blockade of both cyclooxygenase and nitric oxide synthase, inhibition of EDHF with chary

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14

Bryan, Robert M., Junping You, Elke M. Golding, and Sean P. Marrelli. "Endothelium-derived Hyperpolarizing Factor." Anesthesiology 102, no. 6 (June 1, 2005): 1261–77. http://dx.doi.org/10.1097/00000542-200506000-00028.

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There is now strong evidence that an endothelial mechanism, other than nitric oxide or prostacyclin, exists for dilating arteries and arterioles. This third pathway has been named endothelium-derived hyperpolarizing factor (EDHF) and should not be confused with endothelium-derived relaxing factor, which is nitric oxide. Currently, there are several ideas for the mechanism of EDHF, which may vary among vessels of different organs and species. During some pathologic states, EDHF can be up-regulated. This up-regulation often occurs as the dilator effects of endothelium-derived nitric oxide are su

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15

Schildmeyer, Lisa A., and Robert M. Bryan. "Effect of NO on EDHF response in rat middle cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 2 (February 1, 2002): H734—H738. http://dx.doi.org/10.1152/ajpheart.00583.2001.

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Whereas the actual identity of endothelium-derived hyperpolarizing factor (EDHF) is still not certain, it involves a process requiring the endothelium and eliciting hyperpolarization and relaxation of smooth muscle. It is neither nitric oxide (NO) nor prostacyclin, and its presence has been demonstrated in a variety of vessels. Recent studies in peripheral vessels report that EDHF-mediated dilations were either attenuated or blocked by NO. Studies presented here demonstrate that NO does not block EDHF-mediated dilations in cerebral vessels. Rat middle cerebral arteries were cannulated, pressur

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16

Wigg, Susan J., Marianne Tare, Mary A. Tonta, Richard C. O'Brien, Ian T. Meredith, and Helena C. Parkington. "Comparison of effects of diabetes mellitus on an EDHF-dependent and an EDHF-independent artery." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H232—H240. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h232.

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The hypothesis tested in this study is that diabetes has a different impact on an artery in which endothelium-dependent responses derive from both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) compared with responses in which NO predominates and EDHF is absent. The streptozotocin-treated rat model of diabetes was used, and the arteries were mounted on a wire myograph. In mesenteric arteries depolarized and constricted with phenylephrine, acetylcholine evoked hyperpolarization (31 ± 2 mV) and complete relaxation; these responses were attributed to EDHF and NO. In femor

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17

FELETOU, M. "EDHF: new therapeutic targets?" Pharmacological Research 49, no. 6 (June 2004): 565–80. http://dx.doi.org/10.1016/j.phrs.2003.10.017.

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18

PEARSON, J. "Caveolae and EDHF production." Cardiovascular Research 64, no. 2 (November 1, 2004): 189–91. http://dx.doi.org/10.1016/j.cardiores.2004.08.010.

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19

Villar, Inmaculada C., Adrian J. Hobbs, and Amrita Ahluwalia. "Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor." Journal of Endocrinology 197, no. 3 (March 31, 2008): 447–62. http://dx.doi.org/10.1677/joe-08-0070.

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The vascular endothelium plays a crucial role in the regulation of vascular homeostasis by controlling vascular tone, coagulation, and inflammatory responses. These actions are exerted by endothelial factors including nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The greater incidence of cardiovascular disease (CVD) in men and postmenopausal women compared with premenopausal women implies a vasoprotective phenotype of females, which may be influenced by sex hormones. These hormones, particularly estrogen, have modulatory effects on the endothelium and circu

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20

Loeb, A. L., I. Godeny, and D. E. Longnecker. "Anesthetics alter relative contributions of NO and EDHF in rat cremaster muscle microcirculation." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H618—H627. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h618.

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The contributions of the vasodilators nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rat cremaster muscle microcirculation during halothane, isoflurane, or ketamine anesthesia. After inhibition of prostaglandin synthesis with indomethacin, changes in diameter of fourth-order arterioles to acetylcholine (ACh) or bradykinin (BK) were studied in the presence or absence of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, and/or 20 mM K+, an inhibitor of EDHF action. L-NMMA inhibited ACh- and BK-induced vasodilation during isoflurane

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21

Matsumoto, Takayuki, Tsuneo Kobayashi, and Katsuo Kamata. "Alterations in EDHF-type relaxation and phosphodiesterase activity in mesenteric arteries from diabetic rats." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (July 2003): H283—H291. http://dx.doi.org/10.1152/ajpheart.00954.2002.

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In isolated superior mesenteric artery rings from age-matched control rats and streptozotocin (STZ)-induced diabetic rats, we investigated the role of cAMP in endothelium-derived hyperpolarizing factor (EDHF)-type relaxation. The ACh-induced EDHF-type relaxation was significantly weaker in STZ-induced diabetic rats than in control rats, and in both groups of rats it was attenuated by 18α-glycyrrhetinic acid (18α-GA), an inhibitor of gap junctions, and enhanced by IBMX, a cAMP-phosphodiesterase (PDE) inhibitor. These enhanced EDHF-type responses were very similar in magnitude between diabetic a

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22

Tomioka, Hiroshi, Yuichi Hattori, Mitsuhiro Fukao, Hiroshi Watanabe, Yasuhiro Akaishi, Atsushi Sato, Tran Quang Kim, Ichiro Sakuma, Akira Kitabatake, and Morio Kanno. "Role of endothelial Ni2+-sensitive Ca2+entry pathway in regulation of EDHF in porcine coronary artery." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H730—H737. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h730.

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Elevation of intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells is proposed to be required for generation of vascular actions of endothelium-derived hyperpolarizing factor (EDHF). This study was designed to determine the endothelial Ca2+ source that is important in development of EDHF-mediated vascular actions. In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N G-nitro-l-arginine (l-NNA). The l-NNA-resistant relaxant responses were inhibited by high K+, indicating an invo

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Cheng, Zhongjian, Xiaohua Jiang, Warren D. Kruger, Domenico Praticò, Sapna Gupta, Karthik Mallilankaraman, Muniswamy Madesh, et al. "Hyperhomocysteinemia impairs endothelium-derived hyperpolarizing factor–mediated vasorelaxation in transgenic cystathionine beta synthase–deficient mice." Blood 118, no. 7 (August 18, 2011): 1998–2006. http://dx.doi.org/10.1182/blood-2011-01-333310.

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Abstract Hyperhomocysteinemia (HHcy) is associated with endothelial dysfunction (ED), but the mechanism is largely unknown. In this study, we investigated the role and mechanism of HHcy-induced ED in microvasculature in our newly established mouse model of severe HHcy (plasma total homocysteine, 169.5μM). We found that severe HHcy impaired nitric oxide (NO)– and endothelium-derived hyperpolarizing factor (EDHF)–mediated, endothelium-dependent relaxations of small mesenteric arteries (SMAs). Endothelium-independent and prostacyclin-mediated endothelium-dependent relaxations were not changed. A

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Baragatti, Barbara, Michal Laniado Schwartzman, Debora Angeloni, Francesca Scebba, Enrica Ciofini, Daria Sodini, Virginia Ottaviano, et al. "EDHF function in the ductus arteriosus: evidence against involvement of epoxyeicosatrienoic acids and 12S-hydroxyeicosatetraenoic acid." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 6 (December 2009): H2161—H2168. http://dx.doi.org/10.1152/ajpheart.00576.2009.

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We have previously shown (Ref. 2 ) that endothelium-derived hyperpolarizing factor (EDHF) becomes functional in the fetal ductus arteriosus on removal of nitric oxide and carbon monoxide. From this, it was proposed that EDHF originates from a cytochrome P-450 (CYP450)-catalyzed reaction being inhibited by the two agents. Here, we have examined in the mouse ductus whether EDHF can be identified as an arachidonic acid product of a CYP450 epoxygenase and allied pathways. We did not detect transcripts of the mouse CYP2C subfamily in vessel, while CYP2J subfamily transcripts were expressed with CYP

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Osei-Owusu, Patrick, Rasna Sabharwal, Kevin M. Kaltenbronn, Man-Hee Rhee, Mark W. Chapleau, Hans H. Dietrich, and Kendall J. Blumer. "Regulator of G Protein Signaling 2 Deficiency Causes Endothelial Dysfunction and Impaired Endothelium-derived Hyperpolarizing Factor-mediated Relaxation by Dysregulating Gi/o Signaling." Journal of Biological Chemistry 287, no. 15 (February 21, 2012): 12541–49. http://dx.doi.org/10.1074/jbc.m111.332130.

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Regulator of G protein signaling 2 (RGS2) is a GTPase-activating protein for Gq/11α and Gi/oα subunits. RGS2 deficiency is linked to hypertension in mice and humans, although causative mechanisms are not understood. Because endothelial dysfunction and increased peripheral resistance are hallmarks of hypertension, determining whether RGS2 regulates microvascular reactivity may reveal mechanisms relevant to cardiovascular disease. Here we have determined the effects of systemic versus endothelium- or vascular smooth muscle-specific deletion of RGS2 on microvascular contraction and relaxation. Co

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Luksha, Leonid, Henry Nisell, and Karolina Kublickiene. "The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 6 (June 2004): R1102—R1109. http://dx.doi.org/10.1152/ajpregu.00550.2003.

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We studied the importance of endothelium-derived hyperpolarizing factor (EDHF) vs. nitric oxide (NO) and prostacyclin (PGI2) in bradykinin (BK)-induced relaxation in isolated small subcutaneous arteries from normal pregnant women. We also explored the contribution of cytochrome P-450 (CYP450) product of arachidonic acid (AA) metabolism, hydrogen peroxide (H2O2), and gap junctions that have been suggested to be involved in EDHF-mediated responses. Isolated arteries obtained from subcutaneous fat biopsies of normal pregnant women ( n = 30) undergoing planned cesarean section were mounted in a wi

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Nishikawa, Yasuhiro, David W. Stepp, and William M. Chilian. "Nitric oxide exerts feedback inhibition on EDHF-induced coronary arteriolar dilation in vivo." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 2 (August 1, 2000): H459—H465. http://dx.doi.org/10.1152/ajpheart.2000.279.2.h459.

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We tested the hypothesis that nitric oxide (NO) inhibits endothelium-derived hyperpolarizing factor (EDHF)-induced vasodilation via a negative feedback pathway in the coronary microcirculation. Coronary microvascular diameters were measured using stroboscopic fluorescence microangiography. Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked. Specifically, BK (20, 50, and 100 ng · kg−1 · min−1 ic) caused dose-dependent vasodilation similarly before and after administration of N G-m

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Gokina, N. I., O. Y. Kuzina, and A. M. Vance. "Augmented EDHF signaling in rat uteroplacental vasculature during late pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 5 (November 2010): H1642—H1652. http://dx.doi.org/10.1152/ajpheart.00227.2010.

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A successful pregnancy outcome relies on extensive maternal cardiovascular adaptation, including enhanced uteroplacental vasodilator mechanisms. The objective of the present study was to determine the contribution of the endothelium-derived hyperpolarizing factor (EDHF) signaling in pregnancy-enhanced uterine vasodilation, to define the role of Ca2+-activated K+ channels in mediating EDHF effects, and to explore the impact of endothelial Ca2+ signaling in pregnancy-specific upregulation of EDHF. Fura 2-based measurements of smooth muscle cell (SMC) and endothelial cell cytosolic Ca2+ concentra

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AHLUWALIA, Amrita. "To b'EET or not to b'EET? That is the question!" Clinical Science 105, no. 4 (October 1, 2003): 399–401. http://dx.doi.org/10.1042/cs20030232.

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Since the discovery of endothelium-derived hyperpolarizing factor (EDHF), several different candidates and pathways have been proposed as mediators of endothelium-dependent hyperpolarization of vascular smooth muscle. In particular, there has been considerable support for a role for the cytochrome P450 metabolites, the epoxyeicosatrienoic acids (EETs). However, more recently, this hypothesis has come under severe scrutiny. In this issue of Clinical Science, Passauer et al. demonstrate that an EET cannot be EDHF in the human forearm, and add further to the growing belief that an EET is not a ca

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Harrington, Louise S., Martin J. Carrier, Nicola Gallagher, Derek Gilroy, Chris J. Garland, and Jane A. Mitchell. "Elucidation of the temporal relationship between endothelial-derived NO and EDHF in mesenteric vessels." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (September 2007): H1682—H1688. http://dx.doi.org/10.1152/ajpheart.00389.2007.

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Although the endothelium co-generates both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), the relative contribution from each vasodilator is not clear. In studies where the endothelium is stimulated acutely, EDHF responses predominate in small arteries. However, the temporal relationship between endothelial-derived NO and EDHF over more prolonged periods is unclear but of major physiological importance. Here we have used a classical pharmacological approach to show that EDHF is released transiently compared with NO. Acetylcholine (3 × 10−6 mol/l) dilated second- and/o

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Xu, H. L., R. A. Santizo, V. L. Baughman, and D. A. Pelligrino. "Nascent EDHF-mediated cerebral vasodilation in ovariectomized rats is not induced by eNOS dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (November 2003): H2045—H2053. http://dx.doi.org/10.1152/ajpheart.00439.2003.

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In estrogen-depleted [i.e., ovariectomized (Ovx)] animals, an endothelium-derived hyperpolarizing factor (EDHF)-like mechanism may arise to, at least partially, replace endothelial nitric oxide (NO) synthase (eNOS)-derived NO in modulating cerebral arteriolar tone. Additional findings show that eNOS expression and function is restored in estrogen-treated Ovx female rats, while the nascent EDHF-like activity disappears. Because NO has been linked to repression of EDHF activity in the periphery, the current study was undertaken to examine whether the nascent EDHF role in cerebral vessels of Ovx

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Suzuki, H., and G. Chen. "Endothelium-Derived Hyperpolarizing Factor (EDHF): An Endogenous Potassium-Channel Activator." Physiology 5, no. 5 (October 1, 1990): 212–15. http://dx.doi.org/10.1152/physiologyonline.1990.5.5.212.

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Acetylcholine hyperpolarizes the membrane of vascular smooth muscles by increasing potassium permeability, the response being mediated by an endothelium-derived hyperpolarizing factor (EDHF). The membrane hyperpolarization produced by EDHF is therefore one of the components contributing to endothelium-dependent relaxation of vascular smooth muscles.

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Lischke, Volker, Rudi Busse, and Markus Hecker. "Inhalation Anesthetics Inhibit the Release of Endothelium-derived Hyperpolarizing Factor in the Rabbit Carotid Artery." Anesthesiology 83, no. 3 (September 1, 1995): 574–82. http://dx.doi.org/10.1097/00000542-199509000-00017.

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Background Inhalation anesthetics may interfere with the synthesis or action of endothelium-derived vasoactive factors. We investigated the effects of desflurane, enflurane, halothane, isoflurane, and sevoflurane on the release of nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) in the isolated endothelium-intact carotid artery of the rabbit. Methods Isolated segments of the carotid artery were suspended in Krebs-Henseleit solution (37 degrees C) and preconstricted with phenylephrine (1 microM). Relaxations caused by acetylcholine (ACh) (0.03-10 microM) or sodium nitroprussid

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de Wit, Cor, Norbert Esser, Hans-Anton Lehr, Steffen-Sebastian Bolz, and Ulrich Pohl. "Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 5 (May 1, 1999): H1527—H1534. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1527.

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It is unclear to what extent the endothelium-derived hyperpolarizing factor (EDHF) contributes to the control of microcirculatory blood flow in vivo. We analyzed, by intravital microscopy in hamster muscles, the potential role of EDHF along the vascular tree under stimulated (ACh) or basal conditions. Experiments were performed in conscious as well as anesthetized (pentobarbital, urethan) animals. Additionally, cellular effects of the potential EDHF were studied in isolated small arteries. In pentobarbital-anesthetized animals, treatment with N ω-nitro-l-arginine (l-NNA; 30 μmol/l) and indomet

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Matsumoto, Takayuki, Eri Noguchi, Keiko Ishida, Tsuneo Kobayashi, Nobuhiro Yamada, and Katsuo Kamata. "Metformin normalizes endothelial function by suppressing vasoconstrictor prostanoids in mesenteric arteries from OLETF rats, a model of type 2 diabetes." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H1165—H1176. http://dx.doi.org/10.1152/ajpheart.00486.2008.

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We previously reported that in mesenteric arteries from aged Otsuka Long-Evans Tokushima fatty (OLETF) rats (a type 2 diabetes model) endothelium-derived hyperpolarizing factor (EDHF)-type relaxation is impaired while endothelium-derived contracting factor (EDCF)-mediated contraction is enhanced (Matsumoto T, Kakami M, Noguchi E, Kobayashi T, Kamata K. Am J Physiol Heart Circ Physiol 293: H1480–H1490, 2007). Here we investigated whether acute and/or chronic treatment with metformin might improve this imbalance between the effects of the above endothelium-derived factors in mesenteric arteries

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Woodley, N., R. L. Meunier, and J. K. Barclay. "EDHF mediates the relaxation of stretched canine femoral arteries to acetylcholine." Canadian Journal of Physiology and Pharmacology 79, no. 11 (November 1, 2001): 924–31. http://dx.doi.org/10.1139/y01-079.

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To test the hypothesis that mechanically stretched arteries relax to endothelium-derived vasodilators, we challenged endothelium-intact dog femoral artery rings stretched from 1 to 16 g total initial tension (active force and passive elastic) with 106 M acetylcholine (ACh), an endothelium-dependent dilator. The relaxation to 106 M sodium nitroprusside (SNP), an endothelium-independent dilator, increased with the total initial tension. The relaxation to ACh averaged approximately 65% of the relaxation to SNP at total initial tensions of 4 to 16 g. To determine the nature of the endothelial-de

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Quilley, John, and John C. McGiff. "Is EDHF an epoxyeicosatrienoic acid?" Trends in Pharmacological Sciences 21, no. 4 (April 2000): 121–24. http://dx.doi.org/10.1016/s0165-6147(00)01445-0.

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Busse, Rudi, Gillian Edwards, Michel Félétou, Ingrid Fleming, Paul M. Vanhoutte, and Arthur H. Weston. "EDHF: bringing the concepts together." Trends in Pharmacological Sciences 23, no. 8 (August 2002): 374–80. http://dx.doi.org/10.1016/s0165-6147(02)02050-3.

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SUZUKI, HIKARU, GUIFA CHEN, and YOSHIMICHI YAMAMOTO. "Endothelium-Derived Hyperpolarizing Factor (EDHF)." Japanese Circulation Journal 56, no. 2 (1992): 170–74. http://dx.doi.org/10.1253/jcj.56.170.

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Campbell, William B., and David R. Harder. "Prologue: EDHF–what is it?" American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (June 1, 2001): H2413—H2416. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2413.

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Suzuki, Hikaru. "Endothelium-derived hyperpolarizing factor (EDHF)." Journal of Molecular and Cellular Cardiology 24 (May 1992): 43. http://dx.doi.org/10.1016/0022-2828(92)90160-2.

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Matsumoto, Takayuki, Tsuneo Kobayashi, Kentaro Wakabayashi, and Katsuo Kamata. "Cilostazol improves endothelium-derived hyperpolarizing factor-type relaxation in mesenteric arteries from diabetic rats." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H1933—H1940. http://dx.doi.org/10.1152/ajpheart.00303.2005.

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We previously reported that in mesenteric arteries from streptozotocin (STZ)-induced diabetic rats that 1) endothelium-derived hyperpolarizing factor (EDHF)-type relaxation is impaired, possibly due to a reduced action of cAMP via increased phosphodiesterase 3 (PDE3) activity (Matsumoto T, Kobayashi T, and Kamata K. Am J Physiol Heart Circ Physiol 285: H283–H291, 2003) and that 2) PKA activity is decreased (Matsumoto T, Wakabayashi K, Kobayashi T, and Kamata K. Am J Physiol Heart Circ Physiol 287: H1064–H1071, 2004). Here we investigated whether chronic treatment with cilostazol, a PDE3 inhibi

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Burger, Natalie Z., Olga Y. Kuzina, George Osol, and Natalia I. Gokina. "Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca2+." American Journal of Physiology-Endocrinology and Metabolism 296, no. 3 (March 2009): E503—E512. http://dx.doi.org/10.1152/ajpendo.90517.2008.

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Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study explores the role of estrogen in controlling EDHF-mediated vasodilation of uterine resistance arteries of the rat and also analyzes the contribution of endothelial cell (EC) Ca2+ signaling to this process. A parallel study was also performed with mesenteric arteries to provide comparison with a nonreproductive vasculature. Mature female rats underwent ovariectomy, with one half receiving 17β-estradiol replacement (OVX+E) and the other half serving as estroge

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Coleman, H. A., Marianne Tare, and Helena C. Parkington. "EDHF is not K+ but may be due to spread of current from the endothelium in guinea pig arterioles." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (June 1, 2001): H2478—H2483. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2478.

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Endothelium-derived hyperpolarizing factor (EDHF)-attributed hyperpolarizations and relaxations were recorded simultaneously from submucosal arterioles of guinea pigs with the use of intracellular microelectrodes and a video-based system, respectively. Membrane currents were recorded from electrically short segments of arterioles under single-electrode voltage clamp. Substance P evoked an outward current with a current-voltage relationship that was well described by the Goldman-Hodgkin-Katz equation for a K+ current, consistent with the involvement of intermediate- and small-conductance Ca2+-a

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Moreno, Juan Manuel, Rosemary Wangensteen, Juan Sainz, Isabel Rodríguez-Gomez, Virginia Chamorro, Antonio Osuna, and Félix Vargas. "Role of endothelium-derived relaxing factors in the renal response to vasoactive agents in hypothyroid rats." American Journal of Physiology-Endocrinology and Metabolism 285, no. 1 (July 2003): E182—E188. http://dx.doi.org/10.1152/ajpendo.00558.2002.

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This study analyzed the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in the abnormal renal vascular reactivity of hypothyroid rats. Renal responses to vasoconstrictors [VC: phenylephrine (PHE) and ANG II] and vasodilators [VD: ACh, sodium nitroprusside (SNP), and papaverine (PV)] were studied in kidneys from control and hypothyroid rats under normal conditions and after NO or EDHF blockade. NO was blocked by the administration of Nω-nitro-l-arginine methyl ester (l-NAME) and EDHF by the administration of tetraethylammonium (TEA) or by an increased extracellul

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Torondel, B., JM Vila, G. Segarra, P. Lluch, P. Medina, J. Martinez-Leon, J. Ortega, and S. Lluch. "Endothelium-dependent responses in human isolated thyroid arteries from donors." Journal of Endocrinology 181, no. 3 (June 1, 2004): 379–84. http://dx.doi.org/10.1677/joe.0.1810379.

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The functional properties of the endothelium of human thyroid arteries remain unexplored. We investigated the intervention of nitric oxide (NO), prostacyclin (PGI(2)) and endothelium-derived hyperpolarizing factor (EDHF) in the responses to acetylcholine and noradrenaline in isolated thyroid arteries obtained from multi-organ donors. Artery rings were suspended in organ baths for isometric recording of tension. The contribution of NO, PGI(2) and EDHF to endothelium-dependent relaxation was determined by the inhibitory effects of N(G)-monomethyl-L-arginine (L-NMMA), indomethacin, and K(+) chann

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Olmos, L., J. V. Mombouli, S. Illiano, and P. M. Vanhoutte. "cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H865—H870. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h865.

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The relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10(-8) M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F2 alpha, and concentration-relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the e

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Marrelli, Sean P. "Mechanisms of endothelial P2Y1- and P2Y2-mediated vasodilatation involve differential [Ca2+]i responses." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1759—H1766. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1759.

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The present study was designed to evaluate the role of endothelial intracellular Ca2+ concentration ([Ca2+]i) in the difference between P2Y1- and P2Y2-mediated vasodilatations in cerebral arteries. Rat middle cerebral arteries were cannulated, pressurized, and luminally perfused. The endothelium was selectively loaded with fura 2, a fluorescent Ca2+indicator, for simultaneous measurement of endothelial [Ca2+]i and diameter. Luminal administration of 2-methylthioadenosine 5′-triphosphate (2-MeS-ATP), an endothelial P2Y1 agonist, resulted in purely nitric oxide (NO)-dependent dilation and [Ca2+]

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Ogawa, Koji, Satoru Tanaka, and Paul A. Murray. "Inhibitory Effects of Etomidate and Ketamine on Endothelium-dependent Relaxation in Canine Pulmonary Artery." Anesthesiology 94, no. 4 (April 1, 2001): 668–77. http://dx.doi.org/10.1097/00000542-200104000-00022.

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Background The authors recently demonstrated that acetylcholine-induced pulmonary vasorelaxation had two primary components, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). The goal was to investigate the effects of etomidate and ketamine on the NO- and EDHF-mediated components of pulmonary vasorelaxation in response to acetylcholine, bradykinin, and the calcium ionophore, A23187. Methods Canine pulmonary arterial rings with an intact endothelium were suspended in organ chambers for isometric tension recording. The effects of etomidate and ketamine (10(-5) M and 10(-4)

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Golding, Elke M., and Tara E. Kepler. "Role of estrogen in modulating EDHF-mediated dilations in the female rat middle cerebral artery." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (June 1, 2001): H2417—H2423. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2417.

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We tested the hypothesis that endothelium-derived hyperpolarizing factor (EDHF) plays a less dominant role in the female cerebrovasculature. The contribution of EDHF to the ATP-mediated dilation was determined in middle cerebral arteries (MCAs) isolated from male and female rats. Four groups of rats were tested: intact male ( n = 12), intact female ( n= 13), estrogen-treated ovariectomized female ( n = 13), and vehicle-treated ovariectomized female ( n = 20) rats. Maximal dilation to ATP was similar in all groups. However, in the presence of N ω-nitro-l-arginine methyl ester (l-NAME, 3 × 10−5

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