title: Peptidergic modulation of the sympathetic contraction in the rabbit ear artery: effects of temperature.
abstract: 1. The effects of neuropeptide Y, endothelin-1, arginine-vasopressin and angiotensin II on the vascular contraction to sympathetic nerve stimulation were studied in isolated segments, 2 mm long, from the rabbit central ear artery, a cutaneous vessel, during changes in temperature (24 degrees -41 degrees C). 2. Transmural electrical stimulation (1-8 Hz, at supramaximal voltage) produced frequency-dependent contraction, and this response, partially blocked by tetrodotoxin (1 microM) and phentolamine (1 microM), was reduced by cooling (30 degrees C -24 degrees C) and was not modified by warming (41 degrees C), as compared to that recorded at 37 degrees C. 3. Pretreatment with neuropeptide Y (10, 30 and 100 nM) increased in a concentration-dependent manner the vascular contraction to sympathetic stimulation at every temperature studied, but this potentiation was greater during cooling (34 degrees C -24 degrees C) than at 37 degrees C or warming (41 degrees C). 4. Pretreatment with endothelin-1 (3 and 10 nM) or vasopressin (0.1, 0.3 and 1 nM) increased in a concentration-dependent manner the vascular contraction to sympathetic stimulation during cooling (34 degrees C -24 degrees C), but not at 37 degrees C or warming (41 degrees C). 5. Pretreatment with angiotensin II (0.1, 0.3 and 1 microM) did not modify the contraction to sympathetic stimulation at any temperature studied. 6. These results suggest that neuropeptide Y, endothelin-1 and vasopressin, but not angiotensin II, modulate the cutaneous vasoconstriction to sympathetic nerve stimulation by potentiating this vasoconstriction during cooling.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Padilla
authors.forename: A L
authors.initials: AL
authors.lastname: García-Villalón
authors.forename: L
authors.initials: L
authors.lastname: Monge
authors.forename: J L
authors.initials: JL
authors.lastname: García
authors.forename: N
authors.initials: N
authors.lastname: Fernández
authors.forename: B
authors.initials: B
authors.lastname: Gómez
authors.forename: G
authors.initials: G
authors.lastname: Diéguez
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000633:toxicity; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects / Q000378:metabolism; D003080:Cold Temperature; D004305:Dose-Response Relationship, Drug; D004423:Ear / Q000098:blood supply*; D004558:Electric Stimulation; D019332:Endothelin-1 / Q000494:pharmacology; D006358:Hot Temperature; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009478:Neuropeptide Y / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology*; D010646:Phentolamine / Q000633:toxicity; D011817:Rabbits; D013565:Sympatholytics / Q000633:toxicity; D013779:Tetrodotoxin / Q000633:toxicity; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D000317:Adrenergic alpha-Antagonists; D019332:Endothelin-1; D009478:Neuropeptide Y; D010455:Peptides; D013565:Sympatholytics; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D001127:Arginine Vasopressin; D013779:Tetrodotoxin; D010646:Phentolamine