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Institute of Physiology, University of Glasgow.

1. An in vitro preparation of the rabbit knee joint, perfused with oxygenated Locke's solution, was used to study the response of articular blood vessels to electrical stimulation of the joint capsule. 2. Using trains of stimulus pulses of different durations, frequency-response curves were obtained. Electrical stimulation always produced vasoconstriction of joint blood vessels, which increased as a function of both frequency and pulse width. 3. This vasoconstrictor response was neurally mediated as it was markedly inhibited after addition to both bath and perfusate of tetrodotoxin. In addition, the response to field stimulation of the capsule was virtually abolished in animals pretreated with reserpine which depletes sympathetic nerve endings of noradrenaline. 4. The response to electrical stimulation was substantially reduced by the alpha-adrenergic antagonist phenoxybenzamine (10(-5) M), the alpha 1-blocker prazosin (10(-6) M), and by guanethidine (10(-5) M) which inhibits the release of noradrenaline, ATP and neuropeptide Y from sympathetic nerve endings. 5. The attenuation of the vasoconstrictor response to field stimulation by prazosin (10(-6) M) was little altered by addition of the alpha 2-adrenoceptor blocker rauwolscine (10(-6) M) to the perfusate. 6. alpha, beta-Methylene ATP (10(-6) M), a P2-purinoceptor desensitizer, had no effect on the vasoconstrictor response to electrical stimulation. 7. These results indicate that the vasoconstrictor response to electrical stimulation of the rabbit knee joint capsule is mediated via noradrenaline acting upon alpha 1-adrenoceptors.

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				J. J. McDougall Abrogation of {alpha}-adrenergic vasoactivity in chronically inflamed rat knee joints Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R821 - R827. [Abstract] [Full Text] [PDF]