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Adrenergic Control of Rat Pineal NO Synthase
Author(s) -
Schaad Nicolas C.,
Vanecek Jiri,
Kosar Evzen,
Aubry JeanMichel,
Schulz Pierre E.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65020935.x
Subject(s) - prazosin , endocrinology , medicine , pineal gland , phenylephrine , propranolol , adrenergic receptor , adrenergic , antagonist , receptor , adrenergic antagonist , pinealocyte , agonist , neurotransmitter , norepinephrine , biology , chemistry , melatonin , dopamine , blood pressure
We have previously shown that exposure of rats to constant light (LL) induced a decrease in NO synthase (NOS) activity in the pineal gland. We present here the evidence that chronic (5 days) norepinephrine (NE) or isoproterenol treatment prevents the effect of LL and enhances pineal NOS activity in LL animals. This effect of NE appears to be mediated by β‐adrenoceptors, because it was not mimicked by the α‐agonist phenylephrine. Pineal NOS activity was reduced in 16‐h light/8‐h dark animals treated for 4 days with the β‐adrenergic antagonist propranolol but not with the α 1 ‐antagonist prazosin, indicating again an involvement of β‐adrenergic receptor in the control of NOS. Treatment with adrenergic antagonists did not affect cortical NOS activity, suggesting that the control of NOS is different in these two tissues or that the pineal expresses a specific isoform of the enzyme. Taken together, these data suggest that NE controls NOS in the pineal gland through β‐adrenergic receptors. To our knowledge, this represent the first demonstration of a regulation of NOS by a neurotransmitter in the CNS, as assayed under V max conditions.