Proceedings of The Physiological Society

University of Leeds (2002) J Physiol 544P, S007


The contribution of neuropeptide Y to sympathetically evoked vasoconstriction of rat tail artery in vitro

Andrea Law and Christopher D. Johnson

Department of Physiology, School of Medicine, Queen's University Belfast, Medical Biology Centre, 97 Lisburn Road, Belfast BT9 7BL, Northern Ireland

An early study that used neuropeptide Y (NPY) as an agonist suggested that NPY contributes to sympathetically evoked responses in rat tail artery in vitro (Nield, 1987). A recent study using the specific NPY Y1 antagonist, BIBP3226, suggested that neurally released NPY does not contribute to sympathetically evoked responses in this vessel (Duckles et al. 1997). Current studies in rat tail artery from this laboratory showed that small numbers of impulses evoke a contraction that relies more on ATP, and with increased numbers of impulses relies more on noradrenaline (Bradley Johnson, unpublished observations), but it is not known whether NPY affects responses to these stimuli preferentially. Here we examine whether sympathetically released NPY contributes to neurally evoked responses in rat tail artery, and whether any contribution of NPY is influenced by the number of sympathetic impulses.

Tail arteries were excised from humanely killed male Sprague-Dawley rats (250-350 g). Isometric contractile responses to electrical field stimulation were measured in response to several batteries of different impulse numbers (all at the same frequency of 20 Hz, 1 ms pulses, supramaximal) in endothelium-denuded vessels. Experiments were conducted in the presence of NPY and the selective NPY Y1 antagonist, BIBP 3226. Electrically evoked responses were abolished in the presence of tetrodotoxin (1 mM) or guanethidine (10 mM).

NPY had a direct agonist action and potentiated sympathetically mediated responses in a dose-related manner (10-9 to 10-6 M). NPY (75 nM) potentiated responses to very short trains (5 impulses) delivered every minute (4/5 experiments) to 169 ± 30 % of control (mean ± S.E.M.). BIBP 3226 (75 nM) decreased this response to 36 ± 5 % of control (n = 5/5). In the presence of NPY, the response to a couplet (2 impulses) was significantly potentiated by 77 ± 13 % (P < 0.05, ANOVA and SNK; n = 12). The response to a short train (20 impulses) was significantly potentiated, but only to 28 ± 4 % greater than control (P < 0.05). In the presence of BIBP 3226, responses to the couplet (53 ± 10 %) and short train (12 ± 4 %) were significantly reduced (P < 0.05 in each case). In the presence of NPY or BIBP 3226 the couplet was affected significantly more than the train (P < 0.05 in each case, Student's paired t test).

This study confirms a role for endogenously released NPY in sympathetically evoked responses in rat tail artery. As it preferentially affects the responses to a couplet, our data raises the possibility that NPY preferentially affects the actions of sympathetically released ATP in this tissue.

All procedures accord with current UK legislation.

Where applicable, experiments conform with Society ethical requirements