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Peptidergic modulation of the sympathetic contraction in the rabbit ear artery: effects of temperature
Author(s) -
Padilla J,
GarcíaVillalón A L,
Monge L,
García J L,
Fernández N,
Gomez B,
Dieguez G
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701094
Subject(s) - vasoconstriction , medicine , vasopressin , endocrinology , contraction (grammar) , stimulation , phentolamine , angiotensin ii , neuropeptide y receptor , chemistry , endothelin receptor , endothelins , neuropeptide , receptor
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°–41°C). Transmural electrical stimulation (1–8 Hz, at supramaximal voltage) produced frequency‐dependent contraction, and this response, partially blocked by tetrodotoxin (1 μ M ) and phentolamine (1 μ M ), was reduced by cooling (30°C–24°C) and was not modified by warming (41°C), as compared to that recorded at 37°C. Pretreatment with neuropeptide Y (10, 30 and 100 n M ) increased in a concentration‐dependent manner the vascular contraction to sympathetic stimulation at every temperature studied, but this potentiation was greater during cooling (34°C–24°C) than at 37°C or warming (41°C). Pretreatment with endothelin‐1 (3 and 10 n M ) or vasopressin (0.1, 0.3 and 1 n M ) increased in a concentration‐dependent manner the vascular contraction to sympathetic stimulation during cooling (34°C–24°C), but not at 37°C or warming (41°C). Pretreatment with angiotensin II (0.1, 0.3 and 1 μ M ) did not modify the contraction to sympathetic stimulation at any temperature studied. 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.British Journal of Pharmacology (1997) 121 , 21–28; doi: 10.1038/sj.bjp.0701094