Neurogenically evoked cerebral artery constriction is mediated by neuropeptide Y.
We examined the proposal that neuropeptide Y (NPY) released from nerve endings constricts cerebral arteries. Neurogenic vasoconstriction of rabbit basilar arteries is of adrenergic origin but is resistant to blockade by classical alpha-adrenoceptor antagonists. Tetrodotoxin-sensitive contractions of the rabbit basilar artery were elicited by transmural stimulation of nerves. The contractions were inhibited by incubation of tissues with an antiserum to NPY (0.32 microL undiluted immune serum/mL); addition of prazosin (0.1 microM) did not further attenuate the nerve-mediated contraction. The antiserum to NPY also antagonized vasoconstriction due to exogenously administered NPY and was without effect on responses due to histamine or angiotensin. Our results indicate that neurogenic vasoconstriction of the rabbit basilar artery is largely due to the release of NPY and that it is unlikely that other vasoconstrictors contribute significantly to the increased tone.
Department of Pharmacology, University of Vermont, College of Medicine, Burlington 05405-0068.
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I
Laher
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Germann
J A
JA
Bevan
D000818:Animals; D001488:Basilar Artery / Q000187:drug effects; D002536:Cerebral Arteries / Q000187:drug effects*; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D009478:Neuropeptide Y / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects*
D009478:Neuropeptide Y; D006632:Histamine; D011224:Prazosin