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 α-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 μL undiluted immune serum/mL); addition of prazosin (0.1 μM) 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.Key words: cerebral artery, nerves, neuropeptide Y, norepinephrine.

Vagal control of guinea pig tracheal smooth muscle: lack of involvement of VIP or nitric oxide

Contractions of the vagally innervated guinea pig tracheal tube preparation were induced by 1) stimulation of the preganglionic cervical vagus nerve (PGS), 2) activation of postganglionic intrinsic nerves by use of transmural stimulation (TMS) in the presence of hexamethonium, and 3) exogenous application of spasmogens, acetylcholine (ACh) and histamine. Contractions were recorded as increases in intraluminal pressure of the sealed Krebs-filled tube preparation. In the absence of basal tone, contractions induced by both PGS and TMS were monophasic. When the tone was raised with histamine (1 microM), the rapid contractions were followed by a slow relaxation during TMS but not during PGS. There was no evidence for any involvement of the putative inhibitory nonadrenergic noncholinergic neurotransmitters vasoactive intestinal peptide (VIP) and nitric oxide (NO) in the response to PGS, because neither the peptidase alpha-chymotrypsin nor the NO synthase inhibitor NG-nitro-L-arginine affected PGS-induced contractions. However, both alpha-chymotrypsin and NG-nitro-L-arginine facilitated contractions induced by TMS, suggesting that both VIP and NO are involved in responses to TMS. The facilitation of TMS-induced contractions by NG-nitro-L-arginine was unaffected by epithelium removal. Therefore, neither VIP nor NO appears to be released during PGS, but both are released during TMS, and the generation of NO during TMS is independent of the epithelium.