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1

Minagawa, Itaru, Masafumi Fukuda, Hisako Ishige, Hiroshi Kohriki, Masatoshi Shibata, Enoch Y. Park, Tatsuo Kawarasaki, and Tetsuya Kohsaka. "Relaxin-like factor (RLF)/insulin-like peptide 3 (INSL3) is secreted from testicular Leydig cells as a monomeric protein comprising three domains B–C–A with full biological activity in boars." Biochemical Journal 441, no. 1 (December 14, 2011): 265–73. http://dx.doi.org/10.1042/bj20111107.

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RLF (relaxin-like factor), also known as INSL3 (insulin-like peptide 3), is a novel member of the relaxin/insulin gene family that is expressed in testicular Leydig cells. Despite the implicated role of RLF/INSL3 in testis development, its native conformation remains unknown. In the present paper we demonstrate for the first time that boar testicular RLF/INSL3 is isolated as a monomeric structure with full biological activity. Using a series of chromatography steps, the native RLF/INSL3 was highly purified as a single peak in reverse-phase HPLC. MS/MS (tandem MS) analysis of the trypsinized sa
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2

Büllesbach, Erika E., and Christian Schwabe. "Tryptophan B27 in the Relaxin-like Factor (RLF) Is Crucial for RLF Receptor-Binding†." Biochemistry 38, no. 10 (March 1999): 3073–78. http://dx.doi.org/10.1021/bi982687u.

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3

Büllesbach, Erika E., Fredric R. Boockfor, George Fullbright, and Christian Schwabe. "Cryptorchidism induced in normal rats by the relaxin-like factor inhibitor." REPRODUCTION 135, no. 3 (March 2008): 351–55. http://dx.doi.org/10.1530/rep-07-0330.

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Cryptorchidism is a serious problem, which affects 2–5% of the male population. Failure of the testes to descend into the scrotal region impairs germ cell development and is associated with a greater incidence of testicular cancer. The relaxin-like factor (RLF or insulin-like-3) has been shown to be critically important for the timely descent of the testicles in mice. We have discovered that the signal initiation site of the RLF can be eliminated without measurable effects on hormone binding to its receptor and that the resulting RLF derivative is a competitive inhibitor of RLF called RLFi. RL
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4

SIQIN, Mari NAKAI, Tomohiro HAGI, Shinichi KATO, Ali Mohammed PITIA, Mai KOTANI, Yuki ODANAKA, et al. "Partial cDNA sequence of a relaxin-like factor (RLF) receptor, LGR8 and possible existence of the RLF ligand-receptor system in goat testes." Animal Science Journal 81, no. 6 (October 29, 2010): 681–86. http://dx.doi.org/10.1111/j.1740-0929.2010.00801.x.

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5

Boockfor, F. "Relaxin-like factor (RLF) serum concentrations and gubernaculum RLF receptor display in relation to pre- and neonatal development of rats." Reproduction 122, no. 6 (December 1, 2001): 899–906. http://dx.doi.org/10.1530/reprod/122.6.899.

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6

Minagawa, Itaru, Dai Sagata, Ali Mohammed Pitia, Hiroshi Kohriki, Masatoshi Shibata, Hiroshi Sasada, Yoshihisa Hasegawa, and Tetsuya Kohsaka. "Dynamics of insulin-like factor 3 and its receptor expression in boar testes." Journal of Endocrinology 220, no. 3 (March 2014): 247–61. http://dx.doi.org/10.1530/joe-13-0430.

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Relaxin-like factor (RLF), now mainly known as insulin-like factor 3 (INSL3), is essential for testis descent during fetal development; however, its function in the adult testis is still being elucidated. As a major step toward understanding the as-yet-unknown function of INSL3 in boars, this study aimed to develop a time-resolved fluoroimmunoassay for boar INSL3, characterize the dynamics of INSL3 expression during development, and demonstrate the expression of the INSL3 hormone–receptor system in the testis. All samples were collected from Duroc boars. The sensitivity of the assay system est
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7

Büllesbach, Erika E., and Christian Schwabe. "The Mode of Interaction of the Relaxin-like Factor (RLF) with the Leucine-rich Repeat G Protein-activated Receptor 8." Journal of Biological Chemistry 281, no. 36 (July 14, 2006): 26136–43. http://dx.doi.org/10.1074/jbc.m601414200.

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8

Post, Ginell R., Carol Swiderski, Bruce A. Waldrop, Lina Salty, Christopher C. Glembotski, Rob M. F. Wolthuis та Naoki Mochizuki. "Guanine Nucleotide Exchange Factor-like Factor (Rlf) Induces Gene Expression and Potentiates α1-Adrenergic Receptor-induced Transcriptional Responses in Neonatal Rat Ventricular Myocytes". Journal of Biological Chemistry 277, № 18 (14 лютого 2002): 15286–92. http://dx.doi.org/10.1074/jbc.m111844200.

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9

Siqin, Itaru Minagawa, Mitsutoshi Okuno, Kimihiko Yamada, Yasushi Sugawara, Yoshio Nagura, Koh-Ichi Hamano, Enoch Y. Park, Hiroshi Sasada, and Tetsuya Kohsaka. "The active form of goat insulin-like peptide 3 (INSL3) is a single-chain structure comprising three domains B-C-A, constitutively expressed and secreted by testicular Leydig cells." Biological Chemistry 394, no. 9 (September 1, 2013): 1181–94. http://dx.doi.org/10.1515/hsz-2012-0357.

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Abstract Relaxin-like factor (RLF), also called insulin-like peptide 3 (INSL3), is a member of the insulin/relaxin gene family and is produced by testicular Leydig cells. While the understanding of its effects is growing, very little is known about the structural and functional properties of native INSL3. Here, we demonstrate that native INSL3 isolated from goat testes is a single-chain structure with full biological activity, and is constitutively expressed and secreted by Leydig cells. Using a series of chromatography steps, native INSL3 was highly purified as a single 12-kDa peak as reveale
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10

Antonelli, Valeria, Francesca Bernasconi, Yung H. Wong та Lucia Vallar. "Activation of B-Raf and Regulation of the Mitogen-activated Protein Kinase Pathway by the Go α chain". Molecular Biology of the Cell 11, № 4 (квітень 2000): 1129–42. http://dx.doi.org/10.1091/mbc.11.4.1129.

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Many receptors coupled to the pertussis toxin-sensitive Gi/o proteins stimulate the mitogen-activated protein kinase (MAPK) pathway. The role of the α chains of these G proteins in MAPK activation is poorly understood. We investigated the ability of Gαo to regulate MAPK activity by transient expression of the activated mutant Gαo-Q205L in Chinese hamster ovary cells. Gαo-Q205L was not sufficient to activate MAPK but greatly enhanced the response to the epidermal growth factor (EGF) receptor. This effect was not associated with changes in the state of tyrosine phosphorylation of the EGF recepto
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11

Apfel, R., D. Benbrook, E. Lernhardt, M. A. Ortiz, G. Salbert, and M. Pfahl. "A novel orphan receptor specific for a subset of thyroid hormone-responsive elements and its interaction with the retinoid/thyroid hormone receptor subfamily." Molecular and Cellular Biology 14, no. 10 (October 1994): 7025–35. http://dx.doi.org/10.1128/mcb.14.10.7025.

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The steroid/hormone nuclear receptor superfamily comprises several subfamilies of receptors that interact with overlapping DNA sequences and/or related ligands. The thyroid/retinoid hormone receptor subfamily has recently attracted much interest because of the complex network of its receptor interactions. The retinoid X receptors (RXRs), for instance, play a very central role in this subfamily, forming heterodimers with several receptors. Here we describe a novel member of this subfamily that interacts with RXR. Using a v-erbA probe, we obtained a cDNA which encodes a novel 445-amino-acid prot
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12

Apfel, R., D. Benbrook, E. Lernhardt, M. A. Ortiz, G. Salbert, and M. Pfahl. "A novel orphan receptor specific for a subset of thyroid hormone-responsive elements and its interaction with the retinoid/thyroid hormone receptor subfamily." Molecular and Cellular Biology 14, no. 10 (October 1994): 7025–35. http://dx.doi.org/10.1128/mcb.14.10.7025-7035.1994.

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The steroid/hormone nuclear receptor superfamily comprises several subfamilies of receptors that interact with overlapping DNA sequences and/or related ligands. The thyroid/retinoid hormone receptor subfamily has recently attracted much interest because of the complex network of its receptor interactions. The retinoid X receptors (RXRs), for instance, play a very central role in this subfamily, forming heterodimers with several receptors. Here we describe a novel member of this subfamily that interacts with RXR. Using a v-erbA probe, we obtained a cDNA which encodes a novel 445-amino-acid prot
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13

Just, Armin, Andrea J. M. Olson, and William J. Arendshorst. "Dual constrictor and dilator actions of ETB receptors in the rat renal microcirculation: interactions with ETA receptors." American Journal of Physiology-Renal Physiology 286, no. 4 (April 2004): F660—F668. http://dx.doi.org/10.1152/ajprenal.00368.2003.

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The vascular actions of endothelin-1 (ET-1) reflect the combination of vasoconstrictor ETA and ETB receptors on smooth muscle cells and vasodilator ETB receptors on endothelial cells. The present study investigated the contribution of ET receptor subtypes using a comprehensive battery of agonists and antagonists infused directly into the renal artery of anesthetized rats to evaluate the actions of each receptor class alone and their interactions. ET-1 (5 pmol) reduced renal blood flow (RBF) 25 ± 1%. ETA antagonist BQ-123 attenuated this response to a 15 ± 1% decrease in RBF ( P < 0.01), ind
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14

Osmond, David A., and Edward W. Inscho. "P2X1 receptor blockade inhibits whole kidney autoregulation of renal blood flow in vivo." American Journal of Physiology-Renal Physiology 298, no. 6 (June 2010): F1360—F1368. http://dx.doi.org/10.1152/ajprenal.00016.2010.

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In vitro experiments demonstrate that P2X1 receptor activation is important for normal afferent arteriolar autoregulatory behavior, but direct in vivo evidence for this relationship occurring in the whole kidney is unavailable. Experiments were performed to test the hypothesis that P2X1 receptors are important for autoregulation of whole kidney blood flow. Renal blood flow (RBF) was measured in anesthetized male Sprague-Dawley rats before and during P2 receptor blockade with PPADS, P2X1 receptor blockade with IP5I, or A1 receptor blockade with DPCPX. Both P2X1 and A1 receptor stimulation with
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15

Huang, Jiean, Sunila Mahavadi, Wimolpak Sriwai, John R. Grider, and Karnam S. Murthy. "Cross-regulation of VPAC2 receptor desensitization by M3 receptors via PKC-mediated phosphorylation of RKIP and inhibition of GRK2." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 3 (March 2007): G867—G874. http://dx.doi.org/10.1152/ajpgi.00326.2006.

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In gastrointestinal smooth muscle cells, VPAC2 receptor desensitization is exclusively mediated by G protein-coupled receptor kinase 2 (GRK2). The present study examined the mechanisms by which acetylcholine (ACh) acting via M3 receptors regulates GRK2-mediated VPAC2 receptor desensitization in gastric smooth muscle cells. Vasoactive intestinal peptide induced VPAC2 receptor phosphorylation, internalization, and desensitization in both freshly dispersed and cultured smooth muscle cells. Costimulation with ACh in the presence of M2 receptor antagonist (i.e., activation of M3 receptors) inhibite
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16

Stockand, James D., and J. Gary Meszaros. "Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (January 1, 2003): H176—H184. http://dx.doi.org/10.1152/ajpheart.00421.2002.

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Aldosterone plays a pathological role in cardiac fibrosis by directly affecting cardiac fibroblasts. Understanding of the cellular mechanisms of aldosterone action in cardiac fibroblasts, however, is rudimentary. One possibility is that aldosterone promotes proliferation of cardiac fibroblasts by activating specific cellular signaling cascades. The current study tests whether aldosterone stimulates proliferation of isolated adult rat cardiac myofibroblasts (RCF) by activating Kirsten Ras (Ki-RasA) and its effector, the MAPK1/2 cascade. Aldosterone (10 nM) significantly increased RCF proliferat
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17

Thai, Tiffany L., and William J. Arendshorst. "ADP-ribosyl cyclase and ryanodine receptors mediate endothelin ETA and ETB receptor-induced renal vasoconstriction in vivo." American Journal of Physiology-Renal Physiology 295, no. 2 (August 2008): F360—F368. http://dx.doi.org/10.1152/ajprenal.00512.2007.

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ADP-ribosyl cyclase (ADPR cyclase) and ryanodine receptors (RyR) participate in calcium transduction in isolated afferent arterioles. We hypothesized that this signaling pathway is activated by ETA and ETB receptors in the renal vasculature to mediate vasoconstriction in vivo. To test this, we measured acute renal blood flow (RBF) responses to ET-1 in anesthetized rats and mice in the presence and absence of functional ADPR cyclase and/or RyR. Inhibitors of ADPR cyclase (nicotinamide) or RyR (ruthenium red) reduced RBF responses to ET-1 by 44% ( P < 0.04 for both) in Sprague-Dawley rats. Mi
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18

Okuda, Keiko, Yoshiaki Sonoda, and James D. Griffin. "A New Model to Evaluate Signaling of Raf in Hematopoietic Cells." Blood 104, no. 11 (November 16, 2004): 1533. http://dx.doi.org/10.1182/blood.v104.11.1533.1533.

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Abstract The Raf/MEK/ERK pathway is thought to be critical in mediating cell survival and proliferation by cytokine receptors. However, the exact contribution of Raf is complex and not well understood. A better understanding of Raf signaling is important because of the recent observation that B-Raf is frequently mutated in various human cancers. We have generated a new model system that activates Raf directly by linking the extracytoplasmic and transmembrane domains of the erythropoietin receptor (EPOR) with the catalytic domain of Raf (CR3). This synthetic oncogene in which dimerization can b
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19

Imai, N., M. Kashiki, P. D. Woolf, and C. S. Liang. "Comparison of cardiovascular effects of mu- and delta-opioid receptor antagonists in dogs with congestive heart failure." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 1994): H912—H917. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h912.

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We have shown previously that right heart failure (RHF) in dogs is associated with activated endogenous opiate systems, and that administration of the opioid receptor antagonist, naloxone, increases arterial pressure, cardiac contractile function and organ blood flows. To study whether the cardiovascular effects of naloxone are mediated via the mu- or delta-opioid receptors, we administered ICI-154,129, a delta-receptor antagonist, and naloxonazine, a mu-receptor antagonist, to 10 conscious dogs with RHF on 2 separate days. Like naloxone, ICI-154,129 increased mean aortic pressure, cardiac out
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20

Fellner, Robert C., Zhengrong Guan, Anthony K. Cook, David M. Pollock, and Edward W. Inscho. "Endothelin contributes to blunted renal autoregulation observed with a high-salt diet." American Journal of Physiology-Renal Physiology 309, no. 8 (October 15, 2015): F687—F696. http://dx.doi.org/10.1152/ajprenal.00641.2014.

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Autoregulation of renal blood flow (RBF) is an essential function of the renal microcirculation that has been previously shown to be blunted by excessive dietary salt. Endogenous endothelin 1 (ET-1) is increased following a high-salt (HS) diet and contributes to the control of RBF but the differential effects of ET-1 on renal microvessel autoregulation in response to HS remain to be established. We hypothesized that a HS diet increases endothelin receptor activation in normal Sprague-Dawley rats and blunts autoregulation of RBF. The role of ET-1 in the blunted autoregulation produced by a HS d
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21

Morrison, D. K., D. R. Kaplan, S. G. Rhee, and L. T. Williams. "Platelet-derived growth factor (PDGF)-dependent association of phospholipase C-gamma with the PDGF receptor signaling complex." Molecular and Cellular Biology 10, no. 5 (May 1990): 2359–66. http://dx.doi.org/10.1128/mcb.10.5.2359.

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We investigated the interaction of phospholipase C-gamma (PLC-gamma) with wild-type and mutant forms of the platelet-derived growth factor (PDGF) beta-receptor both in vivo and in vitro. After PDGF treatment of CHO cell lines expressing wild-type or either of two mutant (delta Ki and Y825F) PDGF receptors, PLC-gamma became tyrosine phosphorylated and associated with the receptor proteins. The receptor association and tyrosine phosphorylation of PLC-gamma correlated with the ability of these receptors to mediate ligand-induced phosphatidylinositol turnover. However, both the delta Ki and Y825F
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22

Morrison, D. K., D. R. Kaplan, S. G. Rhee, and L. T. Williams. "Platelet-derived growth factor (PDGF)-dependent association of phospholipase C-gamma with the PDGF receptor signaling complex." Molecular and Cellular Biology 10, no. 5 (May 1990): 2359–66. http://dx.doi.org/10.1128/mcb.10.5.2359-2366.1990.

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We investigated the interaction of phospholipase C-gamma (PLC-gamma) with wild-type and mutant forms of the platelet-derived growth factor (PDGF) beta-receptor both in vivo and in vitro. After PDGF treatment of CHO cell lines expressing wild-type or either of two mutant (delta Ki and Y825F) PDGF receptors, PLC-gamma became tyrosine phosphorylated and associated with the receptor proteins. The receptor association and tyrosine phosphorylation of PLC-gamma correlated with the ability of these receptors to mediate ligand-induced phosphatidylinositol turnover. However, both the delta Ki and Y825F
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23

Muszynski, K. W., F. W. Ruscetti, G. Heidecker, U. Rapp, J. Troppmair, J. M. Gooya, and J. R. Keller. "Raf-1 protein is required for growth factor-induced proliferation of hematopoietic cells." Journal of Experimental Medicine 181, no. 6 (June 1, 1995): 2189–99. http://dx.doi.org/10.1084/jem.181.6.2189.

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Raf-1 is a 74-kD serine/threonine kinase located in the cell cytoplasm that is activated by phosphorylation in cells stimulated with a variety of mitogens and growth factors, including hematopoietic growth factors. Using c-raf antisense oligonucleotides to block Raf-1 expression, we have established that Raf-1 is required for hematopoietic growth factor-induced proliferation of murine cell lines stimulated by growth factors whose receptors are members of several different structural classes: (a) the hematopoietin receptor family, including interleukin (IL)-2, IL-3, IL-4, granulocyte colony-sti
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24

Russell, M., S. Winitz, and G. L. Johnson. "Acetylcholine muscarinic m1 receptor regulation of cyclic AMP synthesis controls growth factor stimulation of Raf activity." Molecular and Cellular Biology 14, no. 4 (April 1994): 2343–51. http://dx.doi.org/10.1128/mcb.14.4.2343.

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Acetylcholine muscarinic m2 receptors (m2R) couple to heterotrimeric Gi proteins and activate the Ras/Raf/mitogen-activated protein kinase pathway and phosphatidylinositol 3-kinase in Rat 1a cells. In contrast to the m2R, stimulation of the acetylcholine muscarinic m1 receptor (m1R) does not activate the Ras/Raf/mitogen-activated protein kinase regulatory pathway in Rat 1a cells but rather causes a pronounced inhibition of epidermal growth factor and platelet-derived growth factor receptor activation of Raf. In Rat 1a cells, m1R stimulation of phospholipase C beta and the marked rise in intrac
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25

Russell, M., S. Winitz, and G. L. Johnson. "Acetylcholine muscarinic m1 receptor regulation of cyclic AMP synthesis controls growth factor stimulation of Raf activity." Molecular and Cellular Biology 14, no. 4 (April 1994): 2343–51. http://dx.doi.org/10.1128/mcb.14.4.2343-2351.1994.

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Acetylcholine muscarinic m2 receptors (m2R) couple to heterotrimeric Gi proteins and activate the Ras/Raf/mitogen-activated protein kinase pathway and phosphatidylinositol 3-kinase in Rat 1a cells. In contrast to the m2R, stimulation of the acetylcholine muscarinic m1 receptor (m1R) does not activate the Ras/Raf/mitogen-activated protein kinase regulatory pathway in Rat 1a cells but rather causes a pronounced inhibition of epidermal growth factor and platelet-derived growth factor receptor activation of Raf. In Rat 1a cells, m1R stimulation of phospholipase C beta and the marked rise in intrac
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26

Wilkes, B. M., A. R. Pearl, P. F. Mento, M. E. Maita, C. M. Macica, and E. P. Girardi. "Glomerular endothelin receptors during initiation and maintenance of ischemic acute renal failure in rats." American Journal of Physiology-Renal Physiology 260, no. 1 (January 1, 1991): F110—F118. http://dx.doi.org/10.1152/ajprenal.1991.260.1.f110.

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Glomerular endothelin (ET) receptors were studied in normal Sprague-Dawley rats and in rats with ischemic acute renal failure (ARF) induced by a 60-min occlusion of the left renal artery (right kidney intact). In normal rats ET bound to specific glomerular receptor sites [equilibrium affinity constant (Kd), 46.6 +/- 5.8 pM; receptor number (Ro), 1,167 +/- 160 fmol/mg (n = 7)]. ET infusion (90 ng.kg-1.min-1, intra-arterially) raised mean arterial pressure by 32 +/- 4 mmHg, lowered renal blood flow (RBF) by 62% and glomerular filtration rate (GFR) by 49%, and reduced the number of glomerular ET
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27

Jose, Pedro A., Laureano D. Asico, Gilbert M. Eisner, Felice Pocchiari, Claudio Semeraro, and Robin A. Felder. "Effects of costimulation of dopamine D1- and D2-like receptors on renal function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 4 (October 1, 1998): R986—R994. http://dx.doi.org/10.1152/ajpregu.1998.275.4.r986.

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In vitro studies have suggested that dopamine D1- and D2-like receptors interact to inhibit renal sodium transport. We used Z-1046, a dopamine receptor agonist with the rank-order potency D3 ≥ D4 > D2 > D5 > D1, to test the hypothesis that D1- and D2-like receptors interact to inhibit renal sodium transport in vivo in anesthetized rats. Increasing doses of Z-1046, administered via the right renal artery, increased renal blood flow (RBF), urine flow, and absolute and fractional sodium excretion without affecting glomerular filtration rate. For determination of the dopamine receptor inv
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28

Ortíz, M. Clara, Lourdes A. Fortepiani, Francisco M. Ruiz-Marcos, Noemí M. Atucha, and Joaquín García-Estañ. "Role of AT1 receptors in the renal papillary effects of acute and chronic nitric oxide inhibition." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 3 (March 1, 1998): R760—R766. http://dx.doi.org/10.1152/ajpregu.1998.274.3.r760.

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Nitric oxide (NO) is a vasodilator substance controlling renal papillary blood flow (PBF) in the rat. In this study we have evaluated the role of AT1 angiotensin II receptors as modulators of the whole kidney and papillary vasoconstrictor effects induced by the acute or chronic inhibition of NO synthesis. Experiments have been performed in anesthetized, euvolemic Munich-Wistar rats prepared for the study of renal blood flow (RBF) and PBF. In normal rats, acute administration of the NO synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) increased mean arterial pressure (MAP) and decr
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29

Hildt, Eberhard, and Stefanie Oess. "Identification of Grb2 As a Novel Binding Partner of Tumor Necrosis Factor (TNF) Receptor I." Journal of Experimental Medicine 189, no. 11 (June 7, 1999): 1707–14. http://dx.doi.org/10.1084/jem.189.11.1707.

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Tumor necrosis factor α (TNF-α) is a proinflammatory cytokine. Its pleiotropic biological properties are signaled through two distinct cell surface receptors: the TNF receptor type I (TNFR-I) and the TNF receptor type II. Neither of the two receptors possesses tyrosine kinase activity. A large majority of TNF-α–dependent activities can be mediated by TNFR-I. Recently, c-Raf-1 kinase was identified as an intracellular target of a signal transduction cascade initiated by binding of TNF-α to TNFR-I. However, the mechanism engaged in TNF-α–dependent activation of c-Raf-1 kinase is still enigmatic.
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30

Osawa, Yoko, Peter D. Yim, Dingbang Xu, Reynold A. Panettieri та Charles W. Emala. "Raf-1 kinase mediates adenylyl cyclase sensitization by TNF-α in human airway smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 292, № 6 (червень 2007): L1414—L1421. http://dx.doi.org/10.1152/ajplung.00123.2006.

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Tumor necrosis factor (TNF)-α is a potent inflammatory cytokine implicated in the exacerbation of asthma. Chronic exposure to TNF-α has been reported to induce G protein-coupled receptor desensitization, but adenylyl cyclase sensitization, in airway smooth muscle cells by an unknown mechanism. Cyclic AMP, which is synthesized by adenylyl cyclases in response to G protein-coupled receptor signals, is an important second messenger involved in the regulation of the airway muscle proliferation, migration, and tone. In other cell types, TNF-α receptors transactivate the EGF receptor, which activate
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31

Jensen, Elisa P., Steen S. Poulsen, Hannelouise Kissow, Niels-Henrik Holstein-Rathlou, Carolyn F. Deacon, Boye L. Jensen, Jens J. Holst, and Charlotte M. Sorensen. "Activation of GLP-1 receptors on vascular smooth muscle cells reduces the autoregulatory response in afferent arterioles and increases renal blood flow." American Journal of Physiology-Renal Physiology 308, no. 8 (April 15, 2015): F867—F877. http://dx.doi.org/10.1152/ajprenal.00527.2014.

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Glucagon-like peptide (GLP)-1 has a range of extrapancreatic effects, including renal effects. The mechanisms are poorly understood, but GLP-1 receptors have been identified in the kidney. However, the exact cellular localization of the renal receptors is poorly described. The aim of the present study was to localize renal GLP-1 receptors and describe GLP-1-mediated effects on the renal vasculature. We hypothesized that renal GLP-1 receptors are located in the renal microcirculation and that activation of these affects renal autoregulation and increases renal blood flow. In vivo autoradiograph
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32

Patinha, Daniela, Angelica Fasching, Dora Pinho, António Albino-Teixeira, Manuela Morato, and Fredrik Palm. "Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors." American Journal of Physiology-Renal Physiology 304, no. 5 (March 1, 2013): F614—F622. http://dx.doi.org/10.1152/ajprenal.00285.2012.

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Increased angiotensin II (ANG II) or adenosine can potentiate each other in the regulation of renal hemodynamics and tubular function. Diabetes is characterized by hyperfiltration, yet the roles of ANG II and adenosine receptors for controlling baseline renal blood flow (RBF) or tubular Na+ handling in diabetes is presently unknown. Accordingly, the changes in their functions were investigated in control and 2-wk streptozotocin-diabetic rats after intrarenal infusion of the ANG II AT1 receptor antagonist candesartan, the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCP
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33

Purdy, Kit E., and William J. Arendshorst. "EP1 and EP4receptors mediate prostaglandin E2actions in the microcirculation of rat kidney." American Journal of Physiology-Renal Physiology 279, no. 4 (October 1, 2000): F755—F764. http://dx.doi.org/10.1152/ajprenal.2000.279.4.f755.

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Vasodilator prostaglandin PGE2 protects the kidney from excessive vasoconstriction during contraction of extracellular fluid volume and pathophysiological states. However, it is not yet clear which of the four known E-prostanoid (EP) receptors is localized to resistance vessels and mediates net vasodilation. In the present study, we assessed the presence, signal transduction, and actions of EP receptor subtypes in preglomerular arterioles of Sprague-Dawley rat kidneys. RNA encoding EP1, an EP1-variant, and EP4 receptors was identified by RT-PCR in freshly isolated preglomerular microvessels; c
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34

Felder, R. A., C. C. Felder, G. M. Eisner, and P. A. Jose. "The dopamine receptor in adult and maturing kidney." American Journal of Physiology-Renal Physiology 257, no. 3 (September 1, 1989): F315—F327. http://dx.doi.org/10.1152/ajprenal.1989.257.3.f315.

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Dopamine, like other neurotransmitters, exerts its biological effects by occupation of specific receptor subtypes. The dopamine receptors in the central nervous system and certain endocrine organs are classified into the D1/D2 subtypes. Outside the central nervous system, the dopamine receptors are classified into the DA1/DA2 subtypes. The D1/D2 and DA1/DA2 receptor have marked similarities and some differences, the most notable of which is the lower affinity of the DA dopamine compared with the D dopamine receptor. DA1 receptor activation increases renal blood flow (RBF); stimulation of DA1 a
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35

Kramp, R., P. Fourmanoir, and N. Caron. "Endothelin resets renal blood flow autoregulatory efficiency during acute blockade of NO in the rat." American Journal of Physiology-Renal Physiology 281, no. 6 (December 1, 2001): F1132—F1140. http://dx.doi.org/10.1152/ajprenal.0078.2001.

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First published August 15, 2001; 10.1152/ajprenal.00078.2001.—Renal blood flow (RBF) autoregulatory efficiency may be enhanced during NO inhibition in the rat, as recently reported. Under these conditions, endothelin (ET) synthesis and release may be increased. Our purpose was therefore to determine the role of ET in RBF autoregulatory changes induced by NO inhibition. To address this point, ETA/B receptors were blocked in anesthetized rats with bosentan, or selectively with BQ-610 or BQ-788. NO synthesis was inhibited with N G-nitro-l-arginine methyl ester (l-NAME). Mean arterial pressure (MA
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36

KIM, Jee-Young, Myung-Soon YANG, Chun-Do OH, Kyong-Tai KIM, Mahn Joon HA, Shin-Sung KANG, and Jang-Soo CHUN. "Signalling pathway leading to an activation of mitogen-activated protein kinase by stimulating M3 muscarinic receptor." Biochemical Journal 337, no. 2 (January 8, 1999): 275–80. http://dx.doi.org/10.1042/bj3370275.

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The signalling pathway leading to an activation of mitogen-activated protein (MAP) kinase subtypes Erk-1 and -2 upon stimulation of muscarinic receptor with carbachol in human neuroblastoma SK-N-BE2(C) cells was investigated. Carbachol activated Erk-1/-2 by stimulating M3 muscarinic receptor, as determined by specific antagonists for individual muscarinic receptors. The activation of Erk-1/-2 by carbachol was blocked by the inhibition or down-regulation of protein kinase C (PKC). Among the multiple PKC isoforms expressed in SK-N-BE2(C) cells, only PKCε was activated by the treatment of carbach
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37

Pügge, Carolin, Jai Mediratta, Noah J. Marcus, Harold D. Schultz, Alicia M. Schiller та Irving H. Zucker. "Exercise training normalizes renal blood flow responses to acute hypoxia in experimental heart failure: role of the α1-adrenergic receptor". Journal of Applied Physiology 120, № 3 (1 лютого 2016): 334–43. http://dx.doi.org/10.1152/japplphysiol.00320.2015.

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Recent data suggest that exercise training (ExT) is beneficial in chronic heart failure (CHF) because it improves autonomic and peripheral vascular function. In this study, we hypothesized that ExT in the CHF state ameliorates the renal vasoconstrictor responses to hypoxia and that this beneficial effect is mediated by changes in α1-adrenergic receptor activation. CHF was induced in rabbits. Renal blood flow (RBF) and renal vascular conductance (RVC) responses to 6 min of 5% isocapnic hypoxia were assessed in the conscious state in sedentary (SED) and ExT rabbits with CHF with and without α1-a
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38

Naitoh, M., H. Suzuki, M. Murakami, A. Matsumoto, A. Ichihara, H. Nakamoto, Y. Yamamura, and T. Saruta. "Arginine vasopressin produces renal vasodilation via V2 receptors in conscious dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (October 1, 1993): R934—R942. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r934.

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In conscious dogs, 36-h water deprivation induced a significant increase in renal blood flow (RBF) with elevation of the plasma arginine vasopressin (AVP) concentration to 9.6 +/- 1.8 pg/ml. To simulate such a condition, a mild elevation of plasma AVP was produced by infusing AVP intravenously at a dose of 0.1 ng.kg-1.min-1 for 20 min. The plasma AVP concentration then increased to 6.8 +/- 0.7 pg/ml. This dose of AVP increased the RBF by 21.7 +/- 2.6% and decreased the renal vascular resistance by 18.1 +/- 2.3% without significant changes in mean arterial pressure, cardiac output, or heart rat
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39

Vågnes, Øyvind B., Bjarne M. Iversen, and William J. Arendshorst. "Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production." American Journal of Physiology-Renal Physiology 293, no. 3 (September 2007): F860—F867. http://dx.doi.org/10.1152/ajprenal.00510.2006.

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The relative contributions of vasoconstrictor and of dilator systems are balanced in health. The balance is reset in disease, often favoring a predominant role of vasoconstrictors, perhaps due to positive interactions between constrictor systems. For example, in hypertension, chronic high levels of angiotensin II (ANG II) stimulate the production of thromboxane (TxA2/PGH2) and/or isoprostane that activate constrictor thromboxane prostanoid (TP) receptors in the vasculature. The present study evaluated a modest concentration of ANG II administered acutely into the renal artery on urinary excret
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40

Davis, L. S., S. J. Haleen, A. M. Doherty, W. L. Cody, and J. A. Keiser. "Effects of selective endothelin antagonists on the hemodynamic response to cyclosporin A." Journal of the American Society of Nephrology 4, no. 7 (January 1994): 1448–54. http://dx.doi.org/10.1681/asn.v471448.

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Cyclosporin A (CsA) treatment is associated with hypertension and renal dysfunction. Increased circulating endothelin (ET) has been implicated in this renal dysfunction, which is secondary to renal vasoconstriction and decreases in RBF. The effects of the selective blockade of ETA receptors or the combined blockade of ETA and ETB receptors on the acute hemodynamic response to CsA in anesthetized rats were examined. Rats were pretreated with vehicle, BQ-123 (selective ETA receptor antagonist; 0.6 micron/kg per minute), or BQ-123 and PD 142893 (combined ETA/ETB receptor antagonist; 0.6 micron/kg
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41

Audoly, Laurent P., Xiaoping Ruan, Victoria A. Wagner, Jennifer L. Goulet, Stephen L. Tilley, Beverly H. Koller, Thomas M. Coffman, and William J. Arendshorst. "Role of EP2 and EP3 PGE2receptors in control of murine renal hemodynamics." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (January 1, 2001): H327—H333. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h327.

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The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE2. Specifically, we determined the extent to which the EP2 and EP3 receptor subtypes mediate the actions of PGE2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas
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42

Hoagland, Kimberly M., David A. Maddox, and Douglas S. Martin. "Intrarenal infusion of bradykinin elicits a pressor response in conscious rats via a B2-receptor mechanism." Canadian Journal of Physiology and Pharmacology 77, no. 8 (September 1, 1999): 563–70. http://dx.doi.org/10.1139/y99-054.

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Bradykinin (BK) is a peptide known to activate afferent nerve fibers from the kidney and elicit reflex changes in the cardiovascular system. The present study was specifically designed to test the hypothesis that bradykinin B2 receptors mediated the pressor responses elicited during intrarenal bradykinin administration. Pulsed Doppler flow probes were positioned around the left renal artery to measure renal blood flow (RBF). A catheter, to permit selective intrarenal administration of BK, was advanced into the proximal left renal artery. The femoral artery was cannulated to measure mean arteri
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43

THOMSON, Fiona J., Thomas J. JESS, Colin MOYES, Robin PLEVIN, and Gwyn W. GOULD. "Characterization of the intracellular signalling pathways that underlie growth-factor-stimulated glucose transport in Xenopus oocytes: evidence for ras- and rho-dependent pathways of phosphatidylinositol 3-kinase activation." Biochemical Journal 325, no. 3 (August 1, 1997): 637–43. http://dx.doi.org/10.1042/bj3250637.

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The stimulation of glucose transport is one of the early cellular responses to growth factors and is essential for cell proliferation, yet the molecular processes that underlie this response are poorly defined. The aim of this study was to characterize the role of the low-molecular-mass G-proteins, Ras and Rho, and their downstream targets, Raf protein kinase and phosphatidylinositol 3-kinase, in the regulation of glucose transport in Xenopusoocytes by two distinct growth-factor receptors: the insulin-like growth factor I (IGF-I) tyrosine kinase receptor and the heterotrimeric G-protein-couple
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44

Venegas-Pont, Marcia, Keisa W. Mathis, Radu Iliescu, William H. Ray, Porter H. Glover, and Michael J. Ryan. "Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1286—R1292. http://dx.doi.org/10.1152/ajpregu.00079.2011.

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Inflammation and immune system dysfunction contributes to the development of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that carries a high risk for both renal and cardiovascular disease. While hemodynamic changes that may contribute to increased cardiovascular risk have been reported in humans and animal models of SLE, renal hemodynamics have not been widely studied. The renin-angiotensin system (RAS) plays a central role in renal hemodynamic control, and although RAS blockade is a common therapeutic strategy, the role of
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45

Pezeshki, Zahra, and Mehdi Nematbakhsh. "Sex Differences in the Renal Vascular Responses of AT1 and Mas Receptors in Two-Kidney-One-Clip Hypertension." International Journal of Hypertension 2021 (February 20, 2021): 1–8. http://dx.doi.org/10.1155/2021/8820646.

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Background. The prevalence and severity of hypertension, as well as the activity of the systemic and local renin angiotensin systems (RASs), are gender related, with more symptoms in males than in females. However, the underlying mechanisms are not well understood. In this study, we investigated sex differences in renal vascular responses to angiotensin II (Ang II) administration with and without Ang II type 1 and Mas receptor (AT1R and MasR) antagonists (losartan and A779) in the 2K1C rat model of renovascular hypertension. Methods. Male and female 2K1C rats were divided into 8 experimental g
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46

HATAKEYAMA, Mariko, Shuhei KIMURA, Takashi NAKA, Takuji KAWASAKI, Noriko YUMOTO, Mio ICHIKAWA, Jae-Hoon KIM, et al. "A computational model on the modulation of mitogen-activated protein kinase (MAPK) and Akt pathways in heregulin-induced ErbB signalling." Biochemical Journal 373, no. 2 (July 15, 2003): 451–63. http://dx.doi.org/10.1042/bj20021824.

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ErbB tyrosine kinase receptors mediate mitogenic signal cascade by binding a variety of ligands and recruiting the different cassettes of adaptor proteins. In the present study, we examined heregulin (HRG)-induced signal transduction of ErbB4 receptor and found that the phosphatidylinositol 3′-kinase (PI3K)-Akt pathway negatively regulated the extracellular signal-regulated kinase (ERK) cascade by phosphorylating Raf-1 on Ser259. As the time-course kinetics of Akt and ERK activities seemed to be transient and complex, we constructed a mathematical simulation model for HRG-induced ErbB4 recepto
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47

Lee, Angel W. M., and David J. States. "Both Src-Dependent and -Independent Mechanisms Mediate Phosphatidylinositol 3-Kinase Regulation of Colony-Stimulating Factor 1-Activated Mitogen-Activated Protein Kinases in Myeloid Progenitors." Molecular and Cellular Biology 20, no. 18 (September 15, 2000): 6779–98. http://dx.doi.org/10.1128/mcb.20.18.6779-6798.2000.

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ABSTRACT Colony-stimulating factor 1 (CSF-1) supports the proliferation, survival, and differentiation of bone marrow-derived cells of the monocytic lineage. In the myeloid progenitor 32D cell line expressing CSF-1 receptor (CSF-1R), CSF-1 activation of the extracellular signal-regulated kinase (ERK) pathway is both Ras and phosphatidylinositol 3-kinase (PI3-kinase) dependent. PI3-kinase inhibition did not influence events leading to Ras activation. Using the activity of the PI3-kinase effector, Akt, as readout, studies with dominant-negative and oncogenic Ras failed to place PI3-kinase downst
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48

Helle, Frank, Charlotte Jouzel, Christos Chadjichristos, Sandrine Placier, Martin Flamant, Dominique Guerrot, Hélène François, Jean-Claude Dussaule, and Christos Chatziantoniou. "Improvement of renal hemodynamics during hypertension-induced chronic renal disease: role of EGF receptor antagonism." American Journal of Physiology-Renal Physiology 297, no. 1 (July 2009): F191—F199. http://dx.doi.org/10.1152/ajprenal.00015.2009.

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The present study investigated mechanisms of regression of renal disease after severe proteinuria by focusing on the interaction among EGF receptors, renal hemodynamics, and structural lesions. The nitric oxide (NO) inhibitor NG-nitro-l-arginine-methyl ester (l-NAME) was administered chronically in Sprague-Dawley rats. When proteinuria exceeded 2 g/mmol creatinine, animals were divided into three groups for an experimental period of therapy of 2 wk; in one group, l-NAME was removed to allow reactivation of endogenous NO synthesis; in the two other groups, l-NAME removal was combined with EGF o
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49

Chatziantoniou, C., and W. J. Arendshorst. "Impaired ability of prostaglandins to buffer renal vasoconstriction in genetically hypertensive rats." American Journal of Physiology-Renal Physiology 263, no. 4 (October 1, 1992): F573—F580. http://dx.doi.org/10.1152/ajprenal.1992.263.4.f573.

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The purpose of this study was to gain insight into the mechanism(s) responsible for the exaggerated angiotensin II (ANG II)-induced renal vasoconstriction during the development of hypertension. In previous studies we observed that ANG II produces a twofold larger decrease in renal blood flow (RBF) in spontaneously hypertensive (SHR) compared with Wistar-Kyoto (WKY) rats before but not after cyclooxygenase inhibition. We suggested that this strain difference could be attributed to differences in renal prostaglandin (PG) levels and/or action. To evaluate these possibilities, measurements of RBF
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50

Yang, Chih-Ching, Chiang-Ting Chien, Ming-Hsiou Wu, Ming-Chieh Ma, and Chau-Fong Chen. "NMDA receptor blocker ameliorates ischemia-reperfusion-induced renal dysfunction in rat kidneys." American Journal of Physiology-Renal Physiology 294, no. 6 (June 2008): F1433—F1440. http://dx.doi.org/10.1152/ajprenal.00481.2007.

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N-methyl-d-aspartate (NMDA) receptor activated by glutamate/glycine is located in the kidneys. The NMDA receptor subunit NR1 is increased in damaged renal tissue. This study explored the role of NMDA receptors in ischemia-reperfusion-induced renal dysfunction in rats. With Western blot analysis and renal functional assay, NMDA receptor expression was evaluated, as well as its functional role in female Wistar rat kidneys after 45 min of unilateral ischemia followed by 24 h of reperfusion. The effects of intrarenal NMDA receptor agonist and antagonist on renal blood flow (RBF), glomerular filtra
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