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  • Title: Sympathetic innervation and alpha-adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint.
    Author: Najafipour H, Ferrell WR.
    Journal: Br J Pharmacol; 1993 Jan; 108(1):79-84. PubMed ID: 8094028.
    Abstract:
    1. Experiments were performed to determine the nature of adrenoceptors mediating neurally-induced vasoconstriction of blood vessels in the posterior region of the rabbit knee joint capsule. 2. Electrical stimulation of the posterior articular nerve resulted in frequency-dependent vasoconstriction which was maximal at 10 Hz. This response was mediated predominantly by alpha 2-adrenoceptors as it was only slightly reduced by prazosin administration and was not only abolished but converted into a dilator response by the alpha 2-adrenoceptor antagonist rauwolscine. Further experiments with another specific alpha 1-adrenoceptor antagonist YM-12617 showed that the frequency-response curve in the presence of this antagonist did not differ significantly from control. 3. Neurally-induced vasoconstriction did not appear to have a purinergic component as it was unaffected by the P2x-purinoceptor desensitiser alpha, beta methylene ATP. 4. The rank-order of potency of alpha-adrenoceptor agonists given as a bolus by close intra-arterial injection was: adrenaline = UK-14304 > clonidine > phenylephrine, suggesting that the vasoconstrictor effects were mediated predominantly by postjunctional alpha 2-adrenoceptors. 5. The alpha 2-adrenoceptor antagonist rauwolscine converted the constrictor response to close intra-arterial injection of adrenaline into a dilator response. The vasoconstrictor responses to UK-14304, clonidine and phenylephrine were substantially inhibited by rauwolscine. The alpha 1-adrenoceptor antagonist prazosin failed to inhibit the vasoconstrictor responses to adrenaline, clonidine and UK-14304 and resulted in enhancement of their constrictor effects. 6. The enhancement of the responses to the a, and a2 agonists by prazosin appeared to be specifically related to this agent as administration of YM-12617 did not show such enhancement. The dose-response curves to both clonidine and UK-14304 in the presence of YM-12617 did not differ significantly from control responses. Responses to phenylephrine were significantly reduced by YM-12617, indicating the presence of post-junctional a,-adrenoceptors.7. These results show almost complete reversal of the adrenoceptor profile compared to results obtained in an earlier in vitro study, where responses were mediated predominantly by ax,-adrenoceptors with a small population of postjunctional a2-adrenoceptors (Ferrell & Khoshbaten, 1989). This suggests that the differing environment in vitro may not completely reflect the conditions prevailing in vivo.
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