Source:http://linkedlifedata.com/resource/pubmed/id/10958338
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2000-11-29
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| pubmed:abstractText |
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 degrees C and during cooling (30 degrees C). Electrical field stimulation (4-16 Hz) at 37 degrees C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10(-8), 3x10(-8) and 10(-7) M), this potentiation being greater at 30 degrees C than at 37 degrees 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 degrees C and 30 degrees C, reduced by phentolamine (10(-6) M) at 30 degrees C but not at 37 degrees C, was not modified by the purinoceptor antagonist PPADS (3x10(-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 degrees C and reduced it at 30 degrees C. Neither application of an inhibitor of nitric oxide synthesis, L-Nomega-nitro-arginine (L-NOARG, 10(-4) M), nor endothelium removal modified the potentiating effect of NPY at 37 degrees C or 30 degrees C. NPY (10(-8), 3x10(-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 degrees C but not at 37 degrees 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 degrees C and at 30 degrees C, (2) this potentiating effect of NPY was more marked at 30 degrees C than at 37 degrees C, probably because of greater potentiation of the alpha-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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/BIBP 3226,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Phentolamine,
http://linkedlifedata.com/resource/pubmed/chemical/Purinergic Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/Verapamil
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| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
0031-6768
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
440
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
548-55
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:10958338-Adenosine Triphosphate,
pubmed-meshheading:10958338-Adrenergic alpha-Antagonists,
pubmed-meshheading:10958338-Animals,
pubmed-meshheading:10958338-Arginine,
pubmed-meshheading:10958338-Arteries,
pubmed-meshheading:10958338-Calcium Channel Blockers,
pubmed-meshheading:10958338-Calcium Channels,
pubmed-meshheading:10958338-Cold Temperature,
pubmed-meshheading:10958338-Ear,
pubmed-meshheading:10958338-Electric Stimulation,
pubmed-meshheading:10958338-Endothelium, Vascular,
pubmed-meshheading:10958338-Enzyme Inhibitors,
pubmed-meshheading:10958338-Male,
pubmed-meshheading:10958338-Muscle, Smooth, Vascular,
pubmed-meshheading:10958338-Muscle Contraction,
pubmed-meshheading:10958338-Neuropeptide Y,
pubmed-meshheading:10958338-Nitric Oxide Synthase,
pubmed-meshheading:10958338-Norepinephrine,
pubmed-meshheading:10958338-Phentolamine,
pubmed-meshheading:10958338-Purinergic Antagonists,
pubmed-meshheading:10958338-Rabbits,
pubmed-meshheading:10958338-Receptors, Neuropeptide Y,
pubmed-meshheading:10958338-Skin,
pubmed-meshheading:10958338-Sympathetic Nervous System,
pubmed-meshheading:10958338-Vasoconstriction,
pubmed-meshheading:10958338-Verapamil
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| pubmed:year |
2000
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| pubmed:articleTitle |
Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling.
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| pubmed:affiliation |
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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