RESPONSE OF RABBIT EAR AND FEMORAL ARTERIES TO 5-HYDROXYTRYPTAMINE DURING COOLING

Citation
N. Fernandez et al., RESPONSE OF RABBIT EAR AND FEMORAL ARTERIES TO 5-HYDROXYTRYPTAMINE DURING COOLING, Journal of Pharmacy and Pharmacology, 47(1), 1995, pp. 46-51
Citations number
36
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00223573
Volume
47
Issue
1
Year of publication
1995
Pages
46 - 51
Database
ISI
SICI code
0022-3573(1995)47:1<46:ROREAF>2.0.ZU;2-4
Abstract
The effects of cooling on the response of cutaneous and non-cutaneous arteries to 5-hydroxytryptamine (5-HT) were analysed. Segments 2-mm lo ng from rabbit central ear (cutaneous) and femoral (non-cutaneous) art eries were prepared for isometric tension recording hi an organ bath a t 37 and 24 degrees C (cooling). 5-HT (10(-9) 3 x 10(-4) M) induced co ncentration-dependent contraction of the arteries. The sensitivity and maximal contraction of ear arteries and only the maximal contraction of femoral arteries to this amine were reduced at 24 degrees C. Endoth elium removal or pretreatment with the nitric oxide synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME, 10(-5) M) did not affect t he response at 37 degrees C but reversed the decreased sensitivity at 24 degrees C in ear arteries, and neither procedure modified the react ivity at 24 or 37 degrees C in femoral arteries to 5-HT. At both tempe ratures, the response of ear arteries to 5-HT was shifted to the right by phentolamine (10(-6) M) more than by the 5-HT antagonist, ketanser in (3 x 10(-7) M), and that of femoral arteries was shifted to the rig ht by ketanserin or the 5-HT1/5-HT2 antagonist methysergide (3 x 10(-7 ) M) more than by phentolamine, in arteries with and without endotheli um. These data concur with the proposition that the contraction to 5-H T is mediated mainly by alpha-adrenergic receptors in ear arteries and mainly by 5-HT-ergic receptors in femoral arteries, and suggest that cooling reduces the sensitivity of cutaneous, but nor: of deep arterie s to 5-HT, probably by endothelium-nitric oxide-dependent mechanisms.