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Shigetoshi Chiba - One of the best experts on this subject based on the ideXlab platform.

  • Modification of transmitter release from periarterial nerve terminals by dipyridamole in canine isolated splenic artery.
    Clinical and experimental pharmacology & physiology, 2004
    Co-Authors: Makoto Naito, Xiao-ping Yang, Shigetoshi Chiba
    Abstract:

    1. The aim of the present study was to determine the modulatory effects of dipyridamole on purinergic and Adrenergic Transmission in the canine isolated, perfused splenic artery. 2. Periarterial nerve electrical stimulation readily induced a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X receptor-mediated constriction followed by a prolonged, mainly alpha1-adrenoceptor-mediated response. 3. Exposure of tissues to dipyridamole (0.1-1 micro mol/L) dose-dependently inhibited both the first and second peaks of the vasoconstrictor response at a low frequency of stimulation (1 Hz), whereas at an intermediate frequency of stimulation (4 Hz), the first peak of the response was depressed without any significant effect being observed on the second peak of constriction. 4. At a higher dose (1 micro mol/L) dipyridamole potentiated vasoconstrictor responses to noradrenaline (0.03-1 nmol). At any doses used, dipyridamole had no effect on the vasoconstrictor responses to ATP (0.03-1 micro mol). 5. Tyramine (0.01-0.3 micro mol) induced vasoconstriction in a dose-dependent manner. The dose-response curves for tyramine were shifted to the right following treatment with dipyridamole (0.1-1 micro mol/L). 6. The present results indicate that dipyridamole may inhibit purinergic and Adrenergic Transmission presynaptically, whereas postsynaptically dipyridamole may potentiate the Adrenergic vascular constriction by inhibition of transmitter uptake.

  • Differential effects of ω-conotoxin GVIA, tetrodotoxin and prolonged cold storage on purinergic and Adrenergic Transmission in isolated canine splenic artery
    Journal of Cardiovascular Pharmacology, 2000
    Co-Authors: Xiao-ping Yang, Shigetoshi Chiba
    Abstract:

    Double-peaked vasoconstrictions (biphases of vasoconstrictions) were readily induced in the conditions of 30 s trains of pulses at 1 Hz in the isolated, perfused canine splenic artery. P2X purinoceptors have previously been shown to be involved mainly in the first-peaked response and α 1 -adrenoceptors mostly in the second. The treatment with 10 nM co-conotoxin GVIA (ω-CTX) produced a parallel inhibitory effect on the first- and second-peaked vasoconstrictor responses to nerve stimulation. A submaximal concentration of tetrodotoxin (TTX) (3 nM) did not affect the first peak of constriction, but strongly inhibited the second peak, although a larger dose of TTX (30 nM) abolished either the first- or second-peaked response. On the other hand, after cold storage at 4°C for 7 days, the first-peaked vasoconstriction markedly decreased, whereas the second-peaked response was not significantly modified. In conclusion: (I) ω-CTX-sensitive calcium channels may produce a parallel modulation of purinergic and Adrenergic components of sympathetic coTransmission; (2) TTX-sensitive sodium channels may have a more important role in controlling the Adrenergic rather than purinergic Transmission; and (3) the function of purinergic Transmission of sympathetic nerve might be affected more strongly than that of Adrenergic Transmission in the cold-stored canine splenic artery.

  • Differential effects of omega-conotoxin GVIA, tetrodotoxin and prolonged cold storage on purinergic and Adrenergic Transmission in isolated canine splenic artery.
    Journal of cardiovascular pharmacology, 2000
    Co-Authors: X Yang, Shigetoshi Chiba
    Abstract:

    Double-peaked vasoconstrictions (biphases of vasoconstrictions) were readily induced in the conditions of 30 s trains of pulses at 1 Hz in the isolated, perfused canine splenic artery. P2X purinoceptors have previously been shown to be involved mainfy in the first-peaked response and alpha1-adrenoceptors mostly in the second. The treatment with 10 nM omega-conotoxin GVIA (omega-CTX) produced a parallel inhibitory effect on the first- and second-peaked vasoconstrictor responses to nerve stimulation. A submaximal concentration of tetrodotoxin (TTX) (3 nM) did not affect the first peak of constriction, but strongly inhibited the second peak, although a larger dose of TTX (30 nM) abolished either the first- or second-peaked response. On the other hand, after cold storage at 4 degrees C for 7 days, the first-peaked vasoconstriction markedly decreased, whereas the second-peaked response was not significantly modified. (1) omega-CTX-sensitive calcium channels may produce a parallel modulation of purinergic and Adrenergic components of sympathetic coTransmission; (2) TTX-sensitive sodium channels may have a more important role in controlling the Adrenergic rather than purinergic Transmission; and (3) the function of purinergic Transmission of sympathetic nerve might be affected more strongly than that of Adrenergic Transmission in the cold-stored canine splenic artery.

  • Purinergic and Adrenergic Transmission and their presynaptic modulation in canine isolated perfused splenic arteries
    European journal of pharmacology, 1996
    Co-Authors: Lei-ming Ren, Tokio Nakane, Shigetoshi Chiba
    Abstract:

    Abstract Vasoconstrictions induced by periarterial electrical stimulation were analysed pharmacologically in the canine isolated perfused splenic artery. Phentolamine enhanced the vasoconstrictions at 1 Hz but inhibited those at 10 Hz. Suramin and P2x purinoceptor desensitization with α,β-methylene ATP abolished the phentolamine-enhanced and -resistant vasoconstrictions. α,β-Methylene ATP inhibited the vasoconstrictions at 1 Hz and by exogenous ATP but did not change those at 10 Hz and by exogenous noradrenaline. Suramin reduced the vasoconstrictions by the electrical stimulations and α,β-methylene ATP but did not affect those by exogenous ATP. Prazosin did not affect the vasoconstrictions at 1 Hz but inhibited those at 10 Hz. Rauwolscine enhanced the prazosin-resistant vasoconstrictions. These results suggest that the electrical stimulation at 1 Hz releases purinergic transmitters (ATP or a closely related compound) as a dominant candidate for the vasoconstrictions, and a co-released noradrenaline may inhibit the release of purinergic transmitters through presynaptic α2-adrenoceptors in the canine splenic artery.

Scott Herness - One of the best experts on this subject based on the ideXlab platform.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao-dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the beta agonist isoproterenol and blocked by the beta antagonist propranolol. The alpha agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple alpha (alpha1a, alpha1b, alpha1c, alpha1d, alpha2a, alpha2b, alpha2c) and beta (beta1, beta2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of Physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao‐dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the β agonist isoproterenol and blocked by the β antagonist propranolol. The α agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple α (α1a, α1b, α1c, α1d, α2a, α2b, α2c) and β (β1, β2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.

Xiao‐dong Sun - One of the best experts on this subject based on the ideXlab platform.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of Physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao‐dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the β agonist isoproterenol and blocked by the β antagonist propranolol. The α agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple α (α1a, α1b, α1c, α1d, α2a, α2b, α2c) and β (β1, β2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.

Xiao-dong Sun - One of the best experts on this subject based on the ideXlab platform.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao-dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the beta agonist isoproterenol and blocked by the beta antagonist propranolol. The alpha agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple alpha (alpha1a, alpha1b, alpha1c, alpha1d, alpha2a, alpha2b, alpha2c) and beta (beta1, beta2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.

Namik Kaya - One of the best experts on this subject based on the ideXlab platform.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao-dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the beta agonist isoproterenol and blocked by the beta antagonist propranolol. The alpha agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple alpha (alpha1a, alpha1b, alpha1c, alpha1d, alpha2a, alpha2b, alpha2c) and beta (beta1, beta2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.

  • Adrenergic signalling between rat taste receptor cells.
    The Journal of Physiology, 2002
    Co-Authors: Scott Herness, Fang-li Zhao, Namik Kaya, Tiansheng Shen, Xiao‐dong Sun
    Abstract:

    In taste buds, synaptic Transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to Adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the β agonist isoproterenol and blocked by the β antagonist propranolol. The α agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by Adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple α (α1a, α1b, α1c, α1d, α2a, α2b, α2c) and β (β1, β2) subtypes of Adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that Adrenergic Transmission within the taste bud may play a paracrine role in taste physiology.