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Lars Christian Rump - One of the best experts on this subject based on the ideXlab platform.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y_2-receptors
Naunyn-Schmiedeberg's Archives of Pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [^3H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [^3H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05–1.0 μmol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y_2-receptor antagonist BIIE 0246 (0.1 μmol/l) but not by the NPY-Y_1-receptor antagonist BIBP 3226 (10 μmol/l). ATP (10 μmol/l), a stable analogue ADP-βS (3 μmol/l), and NE (1 μmol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y_1, Y_2, Y_4, Y_5, and y_6 was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y_2-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y2-receptors.
Naunyn-Schmiedeberg's archives of pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [(3)H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [(3)H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05-1.0 micromol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y(2)-receptor antagonist BIIE 0246 (0.1 micromol/l) but not by the NPY-Y(1)-receptor antagonist BIBP 3226 (10 micromol/l). ATP (10 micromol/l), a stable analogue ADP-beta S (3 micromol/l), and NE (1 micromol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y(1), Y(2), Y(4), Y(5), and y(6) was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y(2)-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Acetylcholine release in human Heart Atrium: influence of muscarinic autoreceptors, diabetes, and age.
Circulation, 2001Co-Authors: Vitus Oberhauser, Eckhard Schwertfeger, Tobias Rutz, Friedhelm Beyersdorf, Lars Christian RumpAbstract:Background—An imbalance of sympathetic and parasympathetic drive to the Heart is an important risk factor for cardiac death in patients with coronary Heart disease, diabetes, and renal insufficiency. The amount of neurotransmitter released from peripheral autonomic nerves is modulated by presynaptic receptor systems. In analogy to α-autoreceptors on sympathetic nerves, muscarinic autoreceptors activated by endogenous acetylcholine may exist on parasympathetic nerves in the human Heart. Methods and Results—We developed a technique to study acetylcholine release from human atria and investigated muscarinic autoreceptor function. A pharmacological and molecular approach was used to characterize the subtype involved. Of the 5 muscarinic receptor subtypes cloned, only mRNA encoding for M2- and M3-receptors were detected. Potencies of several muscarinic antagonists against the release-inhibiting effect of the nonselective muscarinic agonist carbachol at the cardiac autoreceptor were correlated with published da...
Ashleigh Sartor - One of the best experts on this subject based on the ideXlab platform.
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VACM-1/cul5 expression in vascular tissue in vivo is induced by water deprivation and its expression in vitro regulates aquaporin-1 concentrations
Cell and Tissue Research, 2012Co-Authors: Alyssa E. Johnson, Isabelle P. Le, Bradley T. Andresen, Joseph Stodola, Gary L. Dewey, Shirley B. Dean, James Resau, Pete Haak, Travis Ruch, Ashleigh SartorAbstract:VACM-1, a cul5 gene product, when overexpressed in vitro, has an antiproliferative effect. In vivo, VACM-1/cul5 is present in tissues involved in the regulation of water balance. Neither proteins targeted for VACM-1/cul5-specific degradation nor factors that may regulate its expression in those tissues have been studied. To identify genes that may be misregulated by VACM-1 cDNA, we performed microarray analysis. Our results indicate that in cos-1 cells transfected with VACM-1 cDNA, mRNA levels for several genes, including AQP1, were decreased when compared to the control group. Our results also indicate that in cos-1 cells transfected with VACM-1 cDNA, endogenous AQP1 protein was decreased about 6-fold when compared to the controls. To test the hypothesis that VACM-1/cul5 may be regulated by conditions that compromise water homeostasis in vivo, we determined if 24 h of water deprivation affects VACM-1/cul5 levels or the effect of VACM-1/cul5 on AQP1. VACM-1 mRNA and protein levels were significantly higher in rat mesenteric arteries, skeletal muscle and the Heart ventricle but not in the Heart Atrium from 24-h water-deprived rats when compared to the controls. Interestingly, 24 h of water deprivation increased modification of VACM-1 by an ubiquitin-like protein, Nedd8, essential for cullin-dependent E3 ligase activity. Although water deprivation did not significantly change AQP1 levels in the mesenteric arteries, AQP1 protein concentrations were inversely correlated with the ratio of the VACM-1 to Nedd8-modified VACM-1. These results suggest that VACM-1/cul5 may regulate endothelial AQP1 concentration both in vivo and in vitro.
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Truncated form of VACM-1/cul-5 with an extended 3' untranslated region stimulates cell growth via a MAPK-dependent pathway.
Biochemical and biophysical research communications, 2006Co-Authors: Ashleigh Sartor, J.b. Kossoris, R. Wilcox, R. Shearer, A.e. Zeneberg, P. Zhao, Inara B. Lazdins, Maria A. Burnatowska-hledinAbstract:We have sequenced a 4.9 kb clone (KLB22) which shares 99% sequence homology with the rabbit vasopressin-activated calcium mobilizing (VACM-1) protein. The 5′ terminus sequence of KLB22 cDNA (nucleotides 1–1961) is continuous and overlapping with nucleotides 1226–3186 of the VACM-1 cDNA sequence. The 3′UTR of KLB22 cDNA extends beyond the 3′UTR of VACM-1 by 2999 nt. KLB22 cDNA encodes a 497 amino acid protein, which putatively begins at Met 284 of the 780 amino acid VACM-1 protein. The in vitro translation of KLB22 cDNA yields a 59 kDa protein. When expressed in cos-1 cells, the truncated VACM-1 protein localizes to the nucleus. KLB22 cDNA transfected cells show increased growth rates and increased levels of phosphorylated MAPK when compared to the vector or to VACM-1 cDNA transfected cells. Finally, in vivo, KLB22 protein expression is tissue specific and can be detected in kidney and in Heart Atrium. These results suggest that truncated VACM-1 cDNA (KLB22) increases cell proliferation through a MAPK pathway.
Anna Goraca - One of the best experts on this subject based on the ideXlab platform.
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Increase in Vasopressin Concentration and Cardiodepressant Activity in the Blood Dialysates From the Sella Turcica During Acute Hypoxia
Endocrine regulations, 2000Co-Authors: Anna GoracaAbstract:Objective. It was previously observed that infusion of angiotensin II, hypertonic saline and Nmethyl-D-aspartic acid (NMDA) causes an increase in vasopressin and cardiodepressant factor release from the posterior pituitary lobe into the blood (GORACA 1998). The aim of present study was to investigate if the cardiodepressant factor and vasopressin are simultaneously released from the pituitary into the blood dialysate during acute hypoxia. Methods. The samples of dialysates of venous blood outflowing from the vicinity of cavernous sinus of the sella turcica were collected in anaesthetized rats. 30-min hypoxia was obtained by increasing the respiratory dead space. The concentration of vasopressin in blood dialysate was determined by radioimmmunoassay, and cardiodepressant activity on spontaneously discharging pacemaker tissue of the right auricle of the right Heart Atrium. Results. Acute hypoxia caused simultaneously an increase in cardiodepressant activity and vasopressin concentration in the blood dialysate outflowing from the vicinity of cavernous sinus of the sella turcica. Conclusions. These data suggest that cardiodepressant factor released together with vasopressin from the posterior pituitary lobe decrease the Heart contraction rate and improves coronary circulation affected by vasopressin release.
Eckhard Schwertfeger - One of the best experts on this subject based on the ideXlab platform.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y_2-receptors
Naunyn-Schmiedeberg's Archives of Pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [^3H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [^3H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05–1.0 μmol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y_2-receptor antagonist BIIE 0246 (0.1 μmol/l) but not by the NPY-Y_1-receptor antagonist BIBP 3226 (10 μmol/l). ATP (10 μmol/l), a stable analogue ADP-βS (3 μmol/l), and NE (1 μmol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y_1, Y_2, Y_4, Y_5, and y_6 was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y_2-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y2-receptors.
Naunyn-Schmiedeberg's archives of pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [(3)H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [(3)H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05-1.0 micromol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y(2)-receptor antagonist BIIE 0246 (0.1 micromol/l) but not by the NPY-Y(1)-receptor antagonist BIBP 3226 (10 micromol/l). ATP (10 micromol/l), a stable analogue ADP-beta S (3 micromol/l), and NE (1 micromol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y(1), Y(2), Y(4), Y(5), and y(6) was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y(2)-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Acetylcholine release in human Heart Atrium: influence of muscarinic autoreceptors, diabetes, and age.
Circulation, 2001Co-Authors: Vitus Oberhauser, Eckhard Schwertfeger, Tobias Rutz, Friedhelm Beyersdorf, Lars Christian RumpAbstract:Background—An imbalance of sympathetic and parasympathetic drive to the Heart is an important risk factor for cardiac death in patients with coronary Heart disease, diabetes, and renal insufficiency. The amount of neurotransmitter released from peripheral autonomic nerves is modulated by presynaptic receptor systems. In analogy to α-autoreceptors on sympathetic nerves, muscarinic autoreceptors activated by endogenous acetylcholine may exist on parasympathetic nerves in the human Heart. Methods and Results—We developed a technique to study acetylcholine release from human atria and investigated muscarinic autoreceptor function. A pharmacological and molecular approach was used to characterize the subtype involved. Of the 5 muscarinic receptor subtypes cloned, only mRNA encoding for M2- and M3-receptors were detected. Potencies of several muscarinic antagonists against the release-inhibiting effect of the nonselective muscarinic agonist carbachol at the cardiac autoreceptor were correlated with published da...
Vitus Oberhauser - One of the best experts on this subject based on the ideXlab platform.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y_2-receptors
Naunyn-Schmiedeberg's Archives of Pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [^3H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [^3H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05–1.0 μmol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y_2-receptor antagonist BIIE 0246 (0.1 μmol/l) but not by the NPY-Y_1-receptor antagonist BIBP 3226 (10 μmol/l). ATP (10 μmol/l), a stable analogue ADP-βS (3 μmol/l), and NE (1 μmol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y_1, Y_2, Y_4, Y_5, and y_6 was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y_2-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Neuropeptide Y inhibits acetylcholine release in human Heart Atrium by activation of Y2-receptors.
Naunyn-Schmiedeberg's archives of pharmacology, 2004Co-Authors: Eckhard Schwertfeger, Thomas Klein, Oliver Vonend, Vitus Oberhauser, Johannes Stegbauer, Lars Christian RumpAbstract:Congestive Heart failure and other cardiac diseases are characterized by increased activity of the sympathetic nervous system, whereas at the same time parasympathetic activity is often suppressed. Such imbalance may be a result of or at least enhanced by presynaptic inhibitory effects of sympathetic neurotransmitters on acetylcholine release. We investigated whether the sympathetic cotransmitters neuropeptide Y (NPY), norepinephrine (NE), and ATP are capable of modulating acetylcholine release in human Heart Atrium. Human atrial appendages were incubated with [(3)H]-choline to label cholinergic transmitter stores and placed in superfusion chambers. Electrical field stimulations (S1, S2) induced a tetrodotoxin-dependent [(3)H]-release, which was taken as an index of endogenous acetylcholine release. NE, NPY, ATP, and a P2-receptor analogue were added before S2. NPY (0.05-1.0 micromol/l) concentration dependently inhibited acetylcholine release. This effect was prevented by the NPY-Y(2)-receptor antagonist BIIE 0246 (0.1 micromol/l) but not by the NPY-Y(1)-receptor antagonist BIBP 3226 (10 micromol/l). ATP (10 micromol/l), a stable analogue ADP-beta S (3 micromol/l), and NE (1 micromol/l) had no effect on acetylcholine release. m-RNA for the NPY-receptor subtypes Y(1), Y(2), Y(4), Y(5), and y(6) was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that the sympathetic neurotransmitter NPY inhibits parasympathetic neurotransmission in the human Heart through activation of presynaptic Y(2)-receptors. NE and ATP seem not to play a role. Since NPY plasma levels are high in chronic Heart failure patients, NPY may be one component leading to impaired parasympathetic neurotransmission in those patients.
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Acetylcholine release in human Heart Atrium: influence of muscarinic autoreceptors, diabetes, and age.
Circulation, 2001Co-Authors: Vitus Oberhauser, Eckhard Schwertfeger, Tobias Rutz, Friedhelm Beyersdorf, Lars Christian RumpAbstract:Background—An imbalance of sympathetic and parasympathetic drive to the Heart is an important risk factor for cardiac death in patients with coronary Heart disease, diabetes, and renal insufficiency. The amount of neurotransmitter released from peripheral autonomic nerves is modulated by presynaptic receptor systems. In analogy to α-autoreceptors on sympathetic nerves, muscarinic autoreceptors activated by endogenous acetylcholine may exist on parasympathetic nerves in the human Heart. Methods and Results—We developed a technique to study acetylcholine release from human atria and investigated muscarinic autoreceptor function. A pharmacological and molecular approach was used to characterize the subtype involved. Of the 5 muscarinic receptor subtypes cloned, only mRNA encoding for M2- and M3-receptors were detected. Potencies of several muscarinic antagonists against the release-inhibiting effect of the nonselective muscarinic agonist carbachol at the cardiac autoreceptor were correlated with published da...
