The Experts below are selected from a list of 168 Experts worldwide ranked by ideXlab platform
Shigetoshi Chiba - One of the best experts on this subject based on the ideXlab platform.
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Different sympathetic–parasympathetic interactions on sinus rate and AV conduction in dog Hearts
European Journal of Pharmacology, 1997Co-Authors: Yasuyuki Furukawa, Masahiro Narita, Manabu Takei, Yasuyuki Karasawa, Akihiro Tada, Hiroshi Zenda, Shigetoshi ChibaAbstract:We investigated the sympathetic-parasympathetic interactions involved in SA nodal pacemaker activity and AV conductivity in the anesthetized dog Heart. Stimulation of the intracardiac parasympathetic nerves to the SA nodal region (SAPS) and Stimulation of the intracardiac parasympathetic nerves to the AV nodal region (AVPS) induced negative chronotropic and dromotropic responses, respectively. Cardiac sympathetic Stimulation, aminophylline, 3-isobutyl-1-methylxanthine (IBMX, a relatively pure nonselective phosphodiesterase inhibitor) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-p iridine-5-carboxylate (Bay k 8644, a Ca2+ channel agonist) increased sinus rate and decreased AV conduction time. Sympathetic Stimulation augmented the negative chronotropic response to SAPS but not the negative dromotropic response to AVPS, IBMX augmented both responses, Bay k 8644 augmented the chronotropic response and attenuated the dromotropic response, and aminophylline did not affect the chronotropic response to SAPS and inhibited the dromotropic response to AVPS. Additionally, when Bay k 8644 directly given via the AV node artery decreased AV conduction time, it attenuated the negative dromotropic response to AVPS and carbachol injected into the AV node artery. These results suggest that the differential sympathetic-parasympathetic interactions on sinus rate and AV conduction are at least partly induced by an interaction between changes in slow inward Ca2+ current or intracellular Ca2+ and the cardiac effects of acetylcholine in the Heart in situ.
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Different sympathetic-parasympathetic interactions on sinus rate and atrioventricular conduction in dog Hearts.
European journal of pharmacology, 1997Co-Authors: Yasuyuki Furukawa, Masahiro Narita, Manabu Takei, Yasuyuki Karasawa, Akihiro Tada, Hiroshi Zenda, Shigetoshi ChibaAbstract:We investigated the sympathetic-parasympathetic interactions involved in SA nodal pacemaker activity and AV conductivity in the anesthetized dog Heart. Stimulation of the intracardiac parasympathetic nerves to the SA nodal region (SAPS) and Stimulation of the intracardiac parasympathetic nerves to the AV nodal region (AVPS) induced negative chronotropic and dromotropic responses, respectively. Cardiac sympathetic Stimulation, aminophylline, 3-isobutyl-1-methylxanthine (IBMX, a relatively pure nonselective phosphodiesterase inhibitor) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-p iridine-5-carboxylate (Bay k 8644, a Ca2+ channel agonist) increased sinus rate and decreased AV conduction time. Sympathetic Stimulation augmented the negative chronotropic response to SAPS but not the negative dromotropic response to AVPS, IBMX augmented both responses, Bay k 8644 augmented the chronotropic response and attenuated the dromotropic response, and aminophylline did not affect the chronotropic response to SAPS and inhibited the dromotropic response to AVPS. Additionally, when Bay k 8644 directly given via the AV node artery decreased AV conduction time, it attenuated the negative dromotropic response to AVPS and carbachol injected into the AV node artery. These results suggest that the differential sympathetic-parasympathetic interactions on sinus rate and AV conduction are at least partly induced by an interaction between changes in slow inward Ca2+ current or intracellular Ca2+ and the cardiac effects of acetylcholine in the Heart in situ.
Mariefrederique Sauvage - One of the best experts on this subject based on the ideXlab platform.
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pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart
European Journal of Pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:Abstract A study was made of the effects of 5-hydroxytryptamine (5-HT) on bradayardia induced in vivo by electrical Stimulation of the vagus nerves in pithed rats pretreated with atenolol. 5-HT significantly decreased vagally induced, but not acetylcholine-induced, bradycardia. The first effect was blocked by methiothepin, ketanserin or methiothepin with ketanserin. When 5-HT 1 and 5-HT 2 receptors were blocked, 5-HT produced an increase in vagally induced bradycardia. Both the inhibition and the potentiation were blocked by simultaneous pretreatment with methiothepin, ketanserin and MDL-72222. The 5-HT 2 receptor agonist m-CPP (1-(3-chlorophenyl) piperazine dihydrochloride) caused an inhibition of vagally induced bradycardia whereas the 5-HT 3 receptor agonist m-CPBG (1-(m-chlorophenyl)biguanide hydrochloride) produced a significant increase. The data suggest the presence of presynaptic and/or ganglionic 5-HT 2 receptors in parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine. The presence of 5-HT 3 receptors is also suggested, Stimulation of which induces the release of acetylcholine.
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Pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart.
European journal of pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:The action of dopamine agonists (apomorphine, bromocriptine, pergolide and quinpirole) on the bradycardia induced in vivo by electrical Stimulation of the vagus nerves was studied in pithed rats pretreated with atenolol. The dopamine agonists decreased significantly the vagal-induced but not the acetylcholine-induced bradycardia. The first effect was blocked by (S)-sulpiride or domperidone but not by yohimbine, prazosin or SCH 23390. Both effects were antagonized by methylatropine. The data suggest the presence of presynaptic and/or ganglionic dopamine DA2 receptors in the parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine.
Yasuyuki Furukawa - One of the best experts on this subject based on the ideXlab platform.
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Different sympathetic–parasympathetic interactions on sinus rate and AV conduction in dog Hearts
European Journal of Pharmacology, 1997Co-Authors: Yasuyuki Furukawa, Masahiro Narita, Manabu Takei, Yasuyuki Karasawa, Akihiro Tada, Hiroshi Zenda, Shigetoshi ChibaAbstract:We investigated the sympathetic-parasympathetic interactions involved in SA nodal pacemaker activity and AV conductivity in the anesthetized dog Heart. Stimulation of the intracardiac parasympathetic nerves to the SA nodal region (SAPS) and Stimulation of the intracardiac parasympathetic nerves to the AV nodal region (AVPS) induced negative chronotropic and dromotropic responses, respectively. Cardiac sympathetic Stimulation, aminophylline, 3-isobutyl-1-methylxanthine (IBMX, a relatively pure nonselective phosphodiesterase inhibitor) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-p iridine-5-carboxylate (Bay k 8644, a Ca2+ channel agonist) increased sinus rate and decreased AV conduction time. Sympathetic Stimulation augmented the negative chronotropic response to SAPS but not the negative dromotropic response to AVPS, IBMX augmented both responses, Bay k 8644 augmented the chronotropic response and attenuated the dromotropic response, and aminophylline did not affect the chronotropic response to SAPS and inhibited the dromotropic response to AVPS. Additionally, when Bay k 8644 directly given via the AV node artery decreased AV conduction time, it attenuated the negative dromotropic response to AVPS and carbachol injected into the AV node artery. These results suggest that the differential sympathetic-parasympathetic interactions on sinus rate and AV conduction are at least partly induced by an interaction between changes in slow inward Ca2+ current or intracellular Ca2+ and the cardiac effects of acetylcholine in the Heart in situ.
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Different sympathetic-parasympathetic interactions on sinus rate and atrioventricular conduction in dog Hearts.
European journal of pharmacology, 1997Co-Authors: Yasuyuki Furukawa, Masahiro Narita, Manabu Takei, Yasuyuki Karasawa, Akihiro Tada, Hiroshi Zenda, Shigetoshi ChibaAbstract:We investigated the sympathetic-parasympathetic interactions involved in SA nodal pacemaker activity and AV conductivity in the anesthetized dog Heart. Stimulation of the intracardiac parasympathetic nerves to the SA nodal region (SAPS) and Stimulation of the intracardiac parasympathetic nerves to the AV nodal region (AVPS) induced negative chronotropic and dromotropic responses, respectively. Cardiac sympathetic Stimulation, aminophylline, 3-isobutyl-1-methylxanthine (IBMX, a relatively pure nonselective phosphodiesterase inhibitor) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-p iridine-5-carboxylate (Bay k 8644, a Ca2+ channel agonist) increased sinus rate and decreased AV conduction time. Sympathetic Stimulation augmented the negative chronotropic response to SAPS but not the negative dromotropic response to AVPS, IBMX augmented both responses, Bay k 8644 augmented the chronotropic response and attenuated the dromotropic response, and aminophylline did not affect the chronotropic response to SAPS and inhibited the dromotropic response to AVPS. Additionally, when Bay k 8644 directly given via the AV node artery decreased AV conduction time, it attenuated the negative dromotropic response to AVPS and carbachol injected into the AV node artery. These results suggest that the differential sympathetic-parasympathetic interactions on sinus rate and AV conduction are at least partly induced by an interaction between changes in slow inward Ca2+ current or intracellular Ca2+ and the cardiac effects of acetylcholine in the Heart in situ.
Asuncion Moran - One of the best experts on this subject based on the ideXlab platform.
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Pharmacological characterization of 5-HT receptors in parasympathetic innervation of rat Heart.
European journal of pharmacology, 1994Co-Authors: Asuncion Moran, C Velasco, M.l. Martin, L. San RomanAbstract:A study was made of the effects of 5-hydroxytryptamine (5-HT) on bradycardia induced in vivo by electrical Stimulation of the vagus nerves in pithed rats pretreated with atenolol. 5-HT significantly decreased vagally induced, but not acetylcholine-induced, bradycardia. The first effect was blocked by methiothepin, ketanserin or methiothepin with ketanserin. When 5-HT1 and 5-HT2 receptors were blocked, 5-HT produced an increase in vagally induced bradycardia. Both the inhibition and the potentiation were blocked by simultaneous pretreatment with methiothepin, ketanserin and MDL-72222. The 5-HT2 receptor agonist m-CPP (1-(3-chlorophenyl) piperazine dihydrochloride) caused an inhibition of vagally induced bradycardia whereas the 5-HT3 receptor agonist m-CPBG (1-(m-chlorophenyl)biguanide hydrochloride) produced a significant increase. The data suggest the presence of presynaptic and/or ganglionic 5-HT2 receptors in parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine. The presence of 5-HT3 receptors is also suggested, Stimulation of which induces the release of acetylcholine.
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pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart
European Journal of Pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:Abstract A study was made of the effects of 5-hydroxytryptamine (5-HT) on bradayardia induced in vivo by electrical Stimulation of the vagus nerves in pithed rats pretreated with atenolol. 5-HT significantly decreased vagally induced, but not acetylcholine-induced, bradycardia. The first effect was blocked by methiothepin, ketanserin or methiothepin with ketanserin. When 5-HT 1 and 5-HT 2 receptors were blocked, 5-HT produced an increase in vagally induced bradycardia. Both the inhibition and the potentiation were blocked by simultaneous pretreatment with methiothepin, ketanserin and MDL-72222. The 5-HT 2 receptor agonist m-CPP (1-(3-chlorophenyl) piperazine dihydrochloride) caused an inhibition of vagally induced bradycardia whereas the 5-HT 3 receptor agonist m-CPBG (1-(m-chlorophenyl)biguanide hydrochloride) produced a significant increase. The data suggest the presence of presynaptic and/or ganglionic 5-HT 2 receptors in parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine. The presence of 5-HT 3 receptors is also suggested, Stimulation of which induces the release of acetylcholine.
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Pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart.
European journal of pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:The action of dopamine agonists (apomorphine, bromocriptine, pergolide and quinpirole) on the bradycardia induced in vivo by electrical Stimulation of the vagus nerves was studied in pithed rats pretreated with atenolol. The dopamine agonists decreased significantly the vagal-induced but not the acetylcholine-induced bradycardia. The first effect was blocked by (S)-sulpiride or domperidone but not by yohimbine, prazosin or SCH 23390. Both effects were antagonized by methylatropine. The data suggest the presence of presynaptic and/or ganglionic dopamine DA2 receptors in the parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine.
Jacques Roquebert - One of the best experts on this subject based on the ideXlab platform.
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pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart
European Journal of Pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:Abstract A study was made of the effects of 5-hydroxytryptamine (5-HT) on bradayardia induced in vivo by electrical Stimulation of the vagus nerves in pithed rats pretreated with atenolol. 5-HT significantly decreased vagally induced, but not acetylcholine-induced, bradycardia. The first effect was blocked by methiothepin, ketanserin or methiothepin with ketanserin. When 5-HT 1 and 5-HT 2 receptors were blocked, 5-HT produced an increase in vagally induced bradycardia. Both the inhibition and the potentiation were blocked by simultaneous pretreatment with methiothepin, ketanserin and MDL-72222. The 5-HT 2 receptor agonist m-CPP (1-(3-chlorophenyl) piperazine dihydrochloride) caused an inhibition of vagally induced bradycardia whereas the 5-HT 3 receptor agonist m-CPBG (1-(m-chlorophenyl)biguanide hydrochloride) produced a significant increase. The data suggest the presence of presynaptic and/or ganglionic 5-HT 2 receptors in parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine. The presence of 5-HT 3 receptors is also suggested, Stimulation of which induces the release of acetylcholine.
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Pharmacological characterization of dopamine receptors in parasympathetic innervation of rat Heart.
European journal of pharmacology, 1991Co-Authors: Jacques Roquebert, Patricia Demichel, Asuncion Moran, Mariefrederique SauvageAbstract:The action of dopamine agonists (apomorphine, bromocriptine, pergolide and quinpirole) on the bradycardia induced in vivo by electrical Stimulation of the vagus nerves was studied in pithed rats pretreated with atenolol. The dopamine agonists decreased significantly the vagal-induced but not the acetylcholine-induced bradycardia. The first effect was blocked by (S)-sulpiride or domperidone but not by yohimbine, prazosin or SCH 23390. Both effects were antagonized by methylatropine. The data suggest the presence of presynaptic and/or ganglionic dopamine DA2 receptors in the parasympathetic innervation of the rat Heart, Stimulation of which inhibits the release of acetylcholine.
