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Adrenoceptor profile of blood vessels in the knee joint of the rabbit.
Author(s) -
Ferrell W R,
Khoshbaten A
Publication year - 1989
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1989.sp017693
Subject(s) - prazosin , phenylephrine , phenoxybenzamine , agonist , vasoconstriction , propranolol , alpha (finance) , isoprenaline , medicine , endocrinology , chemistry , phentolamine , adrenergic receptor , pharmacology , receptor , stimulation , antagonist , blood pressure , surgery , construct validity , patient satisfaction
1. An in vitro preparation of the rabbit knee joint, perfused with oxygenated Locke solution, was used to assess the nature of adrenoceptors within articular blood vessels. 2. Dose/response relationships were obtained to intra‐arterial injection of alpha‐ and beta‐adrenoceptor agonists. 3. Adrenaline and noradrenaline produced a similar pattern of increasing constriction of articular vessels with increasing dose of drug. 4. The alpha 1‐agonist, phenylephrine, also produced dose‐dependent constrictor responses, but the alpha 2‐agonist; clonidine, had no effect. The alpha 2‐agonist UK‐14304 did, however, produce modest vasoconstriction which was not greatly altered by the alpha 1‐blocker prazosin. The constrictor effect of noradrenaline was abolished by both the alpha 1,2‐blocker phenoxybenzamine and by prazosin but not by the alpha 2‐blocker rauwalscine. 5. The beta‐adrenoceptor agonist, isoprenaline, had little effect at a dose of 10(‐6) M or lower, but gave rise to a constrictor effect at higher concentrations. This response was blocked by phenoxybenzamine but not by the beta 1,2‐blocker propranolol, suggesting that the constrictor effect was mediated via alpha‐adrenoceptors. 6. The results suggest that alpha 1‐ and alpha 2‐adrenoceptors are present within articular blood vessels, but that beta‐receptors are absent. The effects of noradrenaline appear to be mediated principally via alpha 1‐adrenoceptors.
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