From the Department of Physiology and Biophysics. Baghiyatollah University of Medical Sciences, Tehran, I.R.lran
Abstract: (4428 Views)
Previous in vitro work on rabbit knee joint vessels showed that vasoconstrictor
effects of nerve stimulation and administration of α-adrenoceptor agonists were
mediated predominantly by α1-adrenoceptors5,9 The present experiments were
performed to assess the nature of α-adrenoceptor subtypes within these blood
vessels in vivo. Dose/response relationships for adrenaline and noradrenaline
produced a similar pattern of increasing constriction of articular vessels with
increasing doses of drug. The u} agonist phenylephrine also produced dosedependent
constrictor responses which were diminished by prazosin. Using the α2
agonists clonidine and UK -14304,responses in vivo differed from those previously
observed in vitro. There was virtually no response to clonidine in vitro while
responses were obvious in vivo. Although UK-14304 was found to have small
effects in vitro, but only at high doses, this agent exerted more potent effects in
vivo, significantly greater than those obtained with phenylephrine. Responses to
the α2 agonists were not altered significantly by prazosin but were reduced by
rauwolscine. Following injection of UK -14304, the constrictor response to nerve
stimulation was reduced.
The results suggest that both α1 and α2 adrenoceptors are present
postjunctionally within articular blood vessels, and also that prejunctional α2
receptors are present which presumably regulate neurotransmitter release from
sympathetic nerve endings in the joint capsule.