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  • 1
    ISSN: 1432-2013
    Keywords: Alpha-adrenoceptor vasoconstriction Cutaneous arteries Nitric oxide Purinoceptor vasoconstriction Y1 receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. In order to analyse the effect of neuropeptide Y (NPY) on the cutaneous vascular response to sympathetic nerve stimulation during cooling, the isometric response of isolated 2-mm segments of the rabbit central ear (cutaneous) artery was recorded at 37°C and during cooling (30°C). Electrical field stimulation (4–16 Hz) at 37°C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10–8, 3×10–8 and 10–7 M), this potentiation being greater at 30°C than at 37°C. The NPY-induced potentiation of the contraction elicited by electrical field stimulation (8 Hz) was abolished by an antagonist of Y1 subtype NPY receptors, BIBP3226 (10–6 M), at 37°C and 30°C, reduced by phentolamine (10–6 M) at 30°C but not at 37°C, was not modified by the purinoceptor antagonist PPADS (3×10–5 M) and was reduced by application of both phentolamine and PPADS at both temperatures. Both NiCl2 (10–3 M) and verapamil (10–5 M) abolished the potentiating effect of NPY at 37°C and reduced it at 30°C. Neither application of an inhibitor of nitric oxide synthesis, l-N ω-nitro-arginine (l-NOARG, 10–4 M), nor endothelium removal modified the potentiating effect of NPY at 37°C or 30°C. NPY (10–8, 3×10–8 and 10–7 M) potentiated in a concentration-dependent way the arterial contraction in response to exogenous noradrenaline (10–8–10–4 M) at 30°C but not at 37°C, and it increased the response to ATP (10–4–10–2 M) at both temperatures. Therefore, in cutaneous (ear) arteries: (1) NPY potentiates the sympathetic response at 37°C and at 30°C, (2) this potentiating effect of NPY was more marked at 30°C than at 37°C, probably because of greater potentiation of the α-adrenoceptor response during cooling, and (3) the potentiating effect of NPY at both temperatures is mediated by NPY receptors of the Y1 subtype, is dependent of Ca2+ channels and is independent of the release of endothelial nitric oxide.
    Type of Medium: Electronic Resource
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