Ear Artery

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Geoffrey Burnstock - One of the best experts on this subject based on the ideXlab platform.

  • Lack of uptake, release and action of UTP at sympathetic perivascular nerve terminals in rabbit Ear Artery.
    European journal of pharmacology, 1998
    Co-Authors: Bernard Saïag, Valliolah Shacoori, Philippe Bodin, Michel Catheline, Geoffrey Burnstock
    Abstract:

    A possible role of uridine 5'-triphosphate (UTP) and uridine at sympathetic nerve terminals was studied in the rabbit Ear Artery after incubation of isolated vessels with [3H]uridine or [3H]noradrenaline. It was found that [3H]uridine was taken up by rabbit Ear Artery. This uptake was largely suppressed after the removal of endothelium and was inhibited by ethidium bromide and dipyridamole. Chemical denervation of the vessels with 6-hydroxydopamine did not reduce the uptake. Following pre-incubation of the isolated vessels with [3H]uridine, there was a release of radioactivity from the superfused rabbit Ear Artery. UTP, UDP, UMP and uridine were detected by thin layer chromatography both in the superfusate and inside the vessels. Transmural electric stimulation (30 V, 5 Hz) induced a contraction of the vessels but did not increase the release of uridine nucleotides into the superfusate. [3H]Noradrenaline was released during electric stimulation and the addition of UTP (100 microM) had no effects on this release. To conclude, this study shows that in contrast to endothelial cells, the sympathetic nerve terminals of the rabbit Ear Artery do not take up uridine and do not release uridine-derived nucleotides. UTP at 100 microM is also unable to modulate the evoked release of noradrenaline. These results mainly confine the role of UTP in endothelium-derived vasodilatation via P2Y2 and/or P2Y4 receptors.

  • evoked noradrenaline release in the rabbit Ear Artery enhancement by purines attenuation by neuropeptide y and lack of effect of calcitonin gene related peptide
    British Journal of Pharmacology, 1994
    Co-Authors: K.i. Maynard, Geoffrey Burnstock
    Abstract:

    1. Adenosine (30 microM) and its analogues 5'-N-ethylcarboxaminoadenosine (5 and 30 microM) and L-phenylisopropyladenosine (5 and 30 microM), potentiated the evoked but not spontaneous release of tritiated noradrenaline in the rabbit central Ear Artery. 2. Prejunctional inhibition of the evoked but not spontaneous release of tritiated noradrenaline by 100 nM neuropeptide Y is greater at 2 min than at 10 min after superfusion of the peptide. 3. Calcitonin gene-related peptide (2.63 to 263 nM) did not affect the evoked or spontaneous release of tritiated noradrenaline in this preparation. 4. These results are discussed in terms of prejunctional modulation of sympathetic transmission in the rabbit central Ear Artery.

  • X-irradiation attenuates relaxant responses in the rabbit Ear Artery.
    British journal of pharmacology, 1992
    Co-Authors: K.i. Maynard, Anne L. Stewart-lee, Pam Milner, Geoffrey Burnstock
    Abstract:

    Abstract 1. The relaxant actions of acetylcholine, substance P and calcitonin gene-related peptide, and the levels of neuropeptide Y and calcitonin gene-related peptide were assessed in the rabbit central Ear Artery 1, 4 and 6 weeks after a single dose of 45 Gy X-irradiation, a dose similar to that used clinically in intraoperative radiotherapy. 2. Relaxant responses induced by acetylcholine and substance P (both endothelium-dependent) and calcitonin gene-related peptide (endothelium-independent) were reduced, and endogenous neuropeptide Y and calcitonin gene-related peptide levels were unaffected after X-irradiation. 3. The mechanism(s) by which a single dose of 45 Gy X-irradiation may selectively damage relaxant, but not direct, contractile responses of the smooth muscle (as we have shown previously) of the rabbit central Ear Artery are discussed.

  • Changes in purinergic responses of the rabbit isolated central Ear Artery after chronic electrical stimulation in vivo.
    British journal of pharmacology, 1992
    Co-Authors: K.i. Maynard, A. Loesch, Geoffrey Burnstock
    Abstract:

    1. The effect of chronic (4-16 days) electrical stimulation (5 Hz, 0.3 ms, 4-10 V) of the great auricular nerve in vivo on sympathetic cotransmission in the rabbit isolated central Ear Artery was examined. 2. Chronic stimulation had no significant effect on frequency-dependent (4-60 Hz) neurogenic contractions or contractile responses induced by exogenous noradrenaline (0.1-300 microM). 3. In contrast, contractions induced by exogenous alpha, beta-methylene ATP (10.0 microM) were significantly decreased in preparations from 16-day stimulated animals in comparison with sham-operated, 4-day and 8-day chronically stimulated animal groups. 4. It is concluded that chronic electrical stimulation of nerves supplying the Ear Artery may lead to the selective alteration of postjunctional P2x-purinoceptor mechanisms, while the effects mediated by post-junctional alpha 1-adrenoceptors remain unchanged.

  • Somatostatin modulates vascular sympathetic neurotransmission in the rabbit Ear Artery.
    European journal of pharmacology, 1991
    Co-Authors: K.i. Maynard, Valerie L. Saville, Geoffrey Burnstock
    Abstract:

    Abstract Somatostatin-like immunoreactivity was localised immunohistochemically in perivascular nerves in the rabbit central Ear Artery. Whilst somatostatin had no direct action on this vessel, it significantly inhibited noradrenaline-induced, but not a,β-methylene ATP-induced, vasoconstriction. Somatostatin also inhibited contractions elicited by electrical field stimulation showing greater effect at low (16 Hz) compared with high (64 Hz) frequencies, and inhibited the release of tritiated noradrenaline in a concentration-dependent manner. These results confirm that somatostatin is a neuroregulatory peptide, and suggest that it is modulating vascular sympathetic cotransmission of the rabbit central Ear Artery by acting both prejunctionally to inhibit transmitter release, and postjunctionally to reduce the action of noradrenaline.

William A. Large - One of the best experts on this subject based on the ideXlab platform.

  • TRPC3 properties of a native constitutively active Ca2+-permeable cation channel in rabbit Ear Artery myocytes
    The FASEB Journal, 2007
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally Prestwich, William A. Large
    Abstract:

    We have previously shown a constitutively active and noradrenaline-evoked Ca2+-permeable cation channel in rabbit Ear Artery myocytes which is proposed to have an important role is setting resting ...

  • TRPC3 properties of a native constitutively active Ca2+‐permeable cation channel in rabbit Ear Artery myocytes
    The Journal of Physiology, 2006
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally A. Prestwich, William A. Large
    Abstract:

    Previously we have described a constitutively active, Ca2+-permeable, non-selective cation channel in freshly dispersed rabbit Ear Artery myocytes which has similar properties to some of the canonical transient receptor potential (TRPC) channel proteins. In the present work we have compared the properties of constitutive channel activity with known properties of TRPC proteins by investigating the effect of selective anti-TRPC antibodies and pharmacological agents on whole-cell and single cation channel activity. Bath application of anti-TRPC3 antibodies markedly reduced channel activity in inside-out patches and also produced a pronounced reduction of both current amplitude and variance of constitutively active whole-cell cation currents whereas anti-TRPC1/4/5/6/7 antibodies had no effect on channel activity. In the presence of antigenic peptide, anti-TRPC3 antibodies had no effect on whole-cell or single cation channel activity. Bath application of flufenamic acid, Gd3+, La3+ and Ca2+ inhibited spontaneous channel activity in outside-out patches with IC50 values of 6.8 μm, 25 nm, 1.5 μm and 0.124 mm, respectively, which are similar values to those against TRPC3 proteins. Immunocytochemical studies combined with confocal microscopy showed expression of TRPC3 proteins in Ear Artery myocytes, and these were predominately distributed at, or close to, the plasma membrane. These data provide strong evidence that native constitutively active cation channels in rabbit Ear Artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins may have an important role in mediating this conductance.

  • TRPC3 properties of a native constitutively active Ca2+-permeable cation channel in rabbit Ear Artery myocytes.
    The Journal of physiology, 2006
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally A. Prestwich, William A. Large
    Abstract:

    Previously we have described a constitutively active, Ca2+-permeable, non-selective cation channel in freshly dispersed rabbit Ear Artery myocytes which has similar properties to some of the canonical transient receptor potential (TRPC) channel proteins. In the present work we have compared the properties of constitutive channel activity with known properties of TRPC proteins by investigating the effect of selective anti-TRPC antibodies and pharmacological agents on whole-cell and single cation channel activity. Bath application of anti-TRPC3 antibodies markedly reduced channel activity in inside-out patches and also produced a pronounced reduction of both current amplitude and variance of constitutively active whole-cell cation currents whereas anti-TRPC1/4/5/6/7 antibodies had no effect on channel activity. In the presence of antigenic peptide, anti-TRPC3 antibodies had no effect on whole-cell or single cation channel activity. Bath application of flufenamic acid, Gd3+, La3+ and Ca2+ inhibited spontaneous channel activity in outside-out patches with IC50 values of 6.8 microm, 25 nm, 1.5 microm and 0.124 mm, respectively, which are similar values to those against TRPC3 proteins. Immunocytochemical studies combined with confocal microscopy showed expression of TRPC3 proteins in Ear Artery myocytes, and these were predominately distributed at, or close to, the plasma membrane. These data provide strong evidence that native constitutively active cation channels in rabbit Ear Artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins may have an important role in mediating this conductance.

K.i. Maynard - One of the best experts on this subject based on the ideXlab platform.

  • evoked noradrenaline release in the rabbit Ear Artery enhancement by purines attenuation by neuropeptide y and lack of effect of calcitonin gene related peptide
    British Journal of Pharmacology, 1994
    Co-Authors: K.i. Maynard, Geoffrey Burnstock
    Abstract:

    1. Adenosine (30 microM) and its analogues 5'-N-ethylcarboxaminoadenosine (5 and 30 microM) and L-phenylisopropyladenosine (5 and 30 microM), potentiated the evoked but not spontaneous release of tritiated noradrenaline in the rabbit central Ear Artery. 2. Prejunctional inhibition of the evoked but not spontaneous release of tritiated noradrenaline by 100 nM neuropeptide Y is greater at 2 min than at 10 min after superfusion of the peptide. 3. Calcitonin gene-related peptide (2.63 to 263 nM) did not affect the evoked or spontaneous release of tritiated noradrenaline in this preparation. 4. These results are discussed in terms of prejunctional modulation of sympathetic transmission in the rabbit central Ear Artery.

  • Changes in purinergic responses of the rabbit isolated central Ear Artery after chronic electrical stimulation in vivo.
    British journal of pharmacology, 1992
    Co-Authors: K.i. Maynard, A. Loesch, Geoffrey Burnstock
    Abstract:

    1. The effect of chronic (4-16 days) electrical stimulation (5 Hz, 0.3 ms, 4-10 V) of the great auricular nerve in vivo on sympathetic cotransmission in the rabbit isolated central Ear Artery was examined. 2. Chronic stimulation had no significant effect on frequency-dependent (4-60 Hz) neurogenic contractions or contractile responses induced by exogenous noradrenaline (0.1-300 microM). 3. In contrast, contractions induced by exogenous alpha, beta-methylene ATP (10.0 microM) were significantly decreased in preparations from 16-day stimulated animals in comparison with sham-operated, 4-day and 8-day chronically stimulated animal groups. 4. It is concluded that chronic electrical stimulation of nerves supplying the Ear Artery may lead to the selective alteration of postjunctional P2x-purinoceptor mechanisms, while the effects mediated by post-junctional alpha 1-adrenoceptors remain unchanged.

  • X-irradiation attenuates relaxant responses in the rabbit Ear Artery.
    British journal of pharmacology, 1992
    Co-Authors: K.i. Maynard, Anne L. Stewart-lee, Pam Milner, Geoffrey Burnstock
    Abstract:

    Abstract 1. The relaxant actions of acetylcholine, substance P and calcitonin gene-related peptide, and the levels of neuropeptide Y and calcitonin gene-related peptide were assessed in the rabbit central Ear Artery 1, 4 and 6 weeks after a single dose of 45 Gy X-irradiation, a dose similar to that used clinically in intraoperative radiotherapy. 2. Relaxant responses induced by acetylcholine and substance P (both endothelium-dependent) and calcitonin gene-related peptide (endothelium-independent) were reduced, and endogenous neuropeptide Y and calcitonin gene-related peptide levels were unaffected after X-irradiation. 3. The mechanism(s) by which a single dose of 45 Gy X-irradiation may selectively damage relaxant, but not direct, contractile responses of the smooth muscle (as we have shown previously) of the rabbit central Ear Artery are discussed.

  • Somatostatin modulates vascular sympathetic neurotransmission in the rabbit Ear Artery.
    European journal of pharmacology, 1991
    Co-Authors: K.i. Maynard, Valerie L. Saville, Geoffrey Burnstock
    Abstract:

    Abstract Somatostatin-like immunoreactivity was localised immunohistochemically in perivascular nerves in the rabbit central Ear Artery. Whilst somatostatin had no direct action on this vessel, it significantly inhibited noradrenaline-induced, but not a,β-methylene ATP-induced, vasoconstriction. Somatostatin also inhibited contractions elicited by electrical field stimulation showing greater effect at low (16 Hz) compared with high (64 Hz) frequencies, and inhibited the release of tritiated noradrenaline in a concentration-dependent manner. These results confirm that somatostatin is a neuroregulatory peptide, and suggest that it is modulating vascular sympathetic cotransmission of the rabbit central Ear Artery by acting both prejunctionally to inhibit transmitter release, and postjunctionally to reduce the action of noradrenaline.

Anthony P. Albert - One of the best experts on this subject based on the ideXlab platform.

  • TRPC3 properties of a native constitutively active Ca2+-permeable cation channel in rabbit Ear Artery myocytes
    The FASEB Journal, 2007
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally Prestwich, William A. Large
    Abstract:

    We have previously shown a constitutively active and noradrenaline-evoked Ca2+-permeable cation channel in rabbit Ear Artery myocytes which is proposed to have an important role is setting resting ...

  • TRPC3 properties of a native constitutively active Ca2+‐permeable cation channel in rabbit Ear Artery myocytes
    The Journal of Physiology, 2006
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally A. Prestwich, William A. Large
    Abstract:

    Previously we have described a constitutively active, Ca2+-permeable, non-selective cation channel in freshly dispersed rabbit Ear Artery myocytes which has similar properties to some of the canonical transient receptor potential (TRPC) channel proteins. In the present work we have compared the properties of constitutive channel activity with known properties of TRPC proteins by investigating the effect of selective anti-TRPC antibodies and pharmacological agents on whole-cell and single cation channel activity. Bath application of anti-TRPC3 antibodies markedly reduced channel activity in inside-out patches and also produced a pronounced reduction of both current amplitude and variance of constitutively active whole-cell cation currents whereas anti-TRPC1/4/5/6/7 antibodies had no effect on channel activity. In the presence of antigenic peptide, anti-TRPC3 antibodies had no effect on whole-cell or single cation channel activity. Bath application of flufenamic acid, Gd3+, La3+ and Ca2+ inhibited spontaneous channel activity in outside-out patches with IC50 values of 6.8 μm, 25 nm, 1.5 μm and 0.124 mm, respectively, which are similar values to those against TRPC3 proteins. Immunocytochemical studies combined with confocal microscopy showed expression of TRPC3 proteins in Ear Artery myocytes, and these were predominately distributed at, or close to, the plasma membrane. These data provide strong evidence that native constitutively active cation channels in rabbit Ear Artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins may have an important role in mediating this conductance.

  • TRPC3 properties of a native constitutively active Ca2+-permeable cation channel in rabbit Ear Artery myocytes.
    The Journal of physiology, 2006
    Co-Authors: Anthony P. Albert, Vladomir Pucovsky, Sally A. Prestwich, William A. Large
    Abstract:

    Previously we have described a constitutively active, Ca2+-permeable, non-selective cation channel in freshly dispersed rabbit Ear Artery myocytes which has similar properties to some of the canonical transient receptor potential (TRPC) channel proteins. In the present work we have compared the properties of constitutive channel activity with known properties of TRPC proteins by investigating the effect of selective anti-TRPC antibodies and pharmacological agents on whole-cell and single cation channel activity. Bath application of anti-TRPC3 antibodies markedly reduced channel activity in inside-out patches and also produced a pronounced reduction of both current amplitude and variance of constitutively active whole-cell cation currents whereas anti-TRPC1/4/5/6/7 antibodies had no effect on channel activity. In the presence of antigenic peptide, anti-TRPC3 antibodies had no effect on whole-cell or single cation channel activity. Bath application of flufenamic acid, Gd3+, La3+ and Ca2+ inhibited spontaneous channel activity in outside-out patches with IC50 values of 6.8 microm, 25 nm, 1.5 microm and 0.124 mm, respectively, which are similar values to those against TRPC3 proteins. Immunocytochemical studies combined with confocal microscopy showed expression of TRPC3 proteins in Ear Artery myocytes, and these were predominately distributed at, or close to, the plasma membrane. These data provide strong evidence that native constitutively active cation channels in rabbit Ear Artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins may have an important role in mediating this conductance.

Bengt Gerdin - One of the best experts on this subject based on the ideXlab platform.

  • Nervous influence on traumatic vasospasm in the rabbit Ear Artery
    Microsurgery, 1991
    Co-Authors: Jonas Wadström, Bengt Gerdin
    Abstract:

    The effects of partial denervation, partial denervation with additional nervous blockade with bupivacaine, and total denervation achieved by amputation and replantation of the Ear on traumatic vasospasm were studied in the rabbit. The central Ear Artery was exposed and compressed in a standardized fashion. The inner diameter was determined by in vivo microscopy using transillumination with cold light. The resulting spasm was assessed in terms of its duration, intensity (reduction of initial diameter), and severity (integrated change in diameter over time). None of the types of denervation had any influence on the vasospasm. The results suggest that the vasospasm is a local phenomenon of the vascular smooth muscle and is not modified by the nervous system.

  • Modulatory effects of topically administered lidocaine and pentobarbital on traumatic vasospasm in the rabbit Ear Artery
    British journal of plastic surgery, 1991
    Co-Authors: Bengt Gerdin
    Abstract:

    Abstract The effect of topical administration of 2 or 20% lidocaine and of 3% pentobarbital on traumatic vasospasm was studied in the central Ear Artery of the rabbit. The inner diameter of the Artery was measured by in vivo microscopy. Vasospasm was induced by a standardised pinch of a 3.2 mm long arterial segment and lasted for 10–20 min. The drugs were given locally at maximal spasm, 1 min after spasm induction. All treatments caused prompt resolution of the vasospasm. This was followed by a plateau phase when the vessel diameter was reduced to about 60% of the initial pre-spasm value as a result of drug-induced vasoconstriction. The vasoconstriction lasted between 40 min and 24 h, depending on the treatment. Twenty per cent lidocaine was most effective, but caused thrombosis in microvessels surrounding the central Ear Artery. It is concluded that topical lidocaine and pentobarbital are both effective in resolving traumatic vasospasm but should only be used after careful consideration, since they also cause a general decrease in vascular diameter.