PHARMACOLOGICAL DIFFERENTIATION OF POSTSYNAPTIC ALPHA-ADRENOCEPTORS IN THE DOG SAPHENOUS-VEIN

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  • 1 January 1984
    • journal article
    • research article
    • Vol. 229  (3) , 712-718
Abstract
The dog saphenous vein has postsynaptic subpopulations of both .alpha.1- and .alpha.2-adrenoceptors which are easily demonstrable using selective agonists and antagonists. Specific .alpha.1- (methoxamine and SKF-89748 [1,2,3,4-tetrahydro-8-methoxy-[5-methylthio]-2-naphthalenamine]) or mixed .alpha.1, .alpha.2 (l-norepinephrine and M7 [5,6-dihydroxy-2-(N,N-dimethylamino)-tetrahydronaphthalene hydrochloride]) agonists as well as the specific .alpha.2-agonist, BHT 920 [2-amino-6-allyl-3,4,7,8-tetrahydro-6H-thiazolo (5,4-d) azepine dihyrochloride], cause concentration-related contraction of this tissue. Maximum contractions produced by .alpha.2-activation are significantly less than maximum contractions produced by .alpha.1- or combined .alpha.1-, .alpha.2-adrenoceptor activation. SKF-89748-induced contractions are competitively inhibited by prazosin (pA2 [competitive antagonistic activity] = 7.74) and rauwolscine (pA2 = 6.63); BHT 920-induced contractions are unaffected by prazosin but inhibited by rauwolscine (pA2 = 8.93). Contractile responses to l-norepinephrine are inhibited by prazosin, rauwolscine or phenoxybenzamine in a manner that suggests that norepinephrine interacts with 2 subtypes of .alpha.-adrenoceptors in this tissue. Evidently, the dog saphenous vein strip is a suitable in vitro preparation for study of drug action at both postsynaptic adrenoceptors inasmuch as either subpopulation of .alpha.-adrenoceptor can be studied independently using specific agonists or antagonists.

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