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. 1993 Jan;108(1):79–84. doi: 10.1111/j.1476-5381.1993.tb13443.x

Sympathetic innervation and alpha-adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint.

H Najafipour 1, W R Ferrell 1
PMCID: PMC1907731  PMID: 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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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