Article date: May 1994
By: K.I. Maynard, G. Burnstock, in Volume 112, Issue 1, pages 123-126
Adenosine (30 μm) and its analogues 5′‐N‐ethylcarboxaminoadenosine (5 and 30 μm) and l‐phenylisopropyladenosine (5 and 30 μm), potentiated the evoked but not spontaneous release of tritiated noradrenaline in the rabbit central ear artery.
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.
Calcitonin gene‐related peptide (2.63 to 263 nm) did not affect the evoked or spontaneous release of tritiated noradrenaline in this preparation.
These results are discussed in terms of prejunctional modulation of sympathetic transmission in the rabbit central ear artery.
Adenosine (30 μm) and its analogues 5′‐N‐ethylcarboxaminoadenosine (5 and 30 μm) and l‐phenylisopropyladenosine (5 and 30 μm), potentiated the evoked but not spontaneous release of tritiated noradrenaline in the rabbit central ear artery.
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.
Calcitonin gene‐related peptide (2.63 to 263 nm) did not affect the evoked or spontaneous release of tritiated noradrenaline in this preparation.
These results are discussed in terms of prejunctional modulation of sympathetic transmission in the rabbit central ear artery.
DOI: 10.1111/j.1476-5381.1994.tb13040.x
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