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Cooling and response to adrenoceptor agonists of rabbit ear and femoral artery: role of the endothelium
Author(s) -
GarcíaVillalón A.L.,
Monge L.,
Montoya J.J.,
García J.L.,
Fernández N.,
Gómez B.,
Diéguez G.
Publication year - 1992
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 - 10.1111/j.1476-5381.1992.tb14401.x
Subject(s) - phenylephrine , prazosin , femoral artery , endothelium , agonist , medicine , endocrinology , yohimbine , stimulation , blood vessel , contraction (grammar) , chemistry , anatomy , receptor , blood pressure , antagonist
1 The effects of cooling on the response of the rabbit central ear (cutaneous) and femoral (non‐cutaneous) arteries to stimulation of adrenoceptors and the role of the endothelium in these effects, were studied in 2 mm long cylindrical segments. 2 Concentration‐response curves for noradrenaline (10 −9 − 3 × 10 −4 m ), phenylephrine (α 1 ‐adrenoceptor agonist, 10 −9 − 3 × 10 −4 m ) and B‐HT 920 (α 2 ‐adrenoceptor agonist, 10 −7 − 10 −3 m ) were recorded isometrically in arteries with and without endothelium at 37°C and at 24°C (cooling). To analyze further the endothelial mechanisms in the responses to adrenoceptor stimulation during cooling, the effects of the adrenoceptor agonists on ear arteries in the presence of N G ‐nitro‐ l ‐arginine methyl esther ( l ‐NAME) (10 −5 m ) were also determined. 3 In every condition tested, the three adrenoceptor agonists produced a concentration‐dependent arterial contraction and the order of potency in ear and femoral arteries was noradrenaline ≥ phenylephrine > B‐HT 920. The response of ear and femoral arteries to phenylephrine or B‐HT 920 was blocked by prazosin (10 −6 m ). Yohimbine (10 −6 m ) decreased slightly the response of ear arteries and increased that of femoral arteries to B‐HT 920. 4 The sensitivity of both ear and femoral arteries to the three adrenoceptor agonists was significantly lower at 24°C than at 37°C. 5 In ear arteries, endothelium removal or treatment with l ‐NAME did not influence the response at 37°C, but did increase it during cooling to adrenoceptor stimulation. In femoral arteries, endothelium removal increased the sensitivity to noradrenaline and, especially, to B‐HT 920 at 37°C, but did not affect the response at 24°C. 6 The results suggest that: (a) rabbit ear and femoral arteries are equipped mainly with α 1 ‐adrenoceptors; (b) at 37°C, the contraction of the ear artery to adrenoceptor agonists is mostly endothelium‐independent, and in the femoral artery the contraction to α 2 ‐adrenoceptor activation is endothelium‐dependent; (c) cooling inhibits the contraction to adrenoceptor agonists in both ear and femoral arteries: in the ear artery probably by increasing the availability of endothelial nitric oxide, but in the femoral artery by depressing the sensitivity of α‐adrenoceptors in the smooth musculature. 7 The results suggest that the endothelium may modulate the adrenoceptor response of cutaneous arteries during changes in temperature.