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pubmed:abstractText |
The present study was undertaken to investigate the effect of alpha(2)-autoreceptor blockade on the facilitatory influence exerted by activation of beta -, A(2A)-adenosine- and angiotensin II receptors. Segments of a rat-tail artery, previously incubated with(3)H-noradrenaline, were subjected to electrical stimulation. The influence of isoprenaline, the compound CGS21680 and angiotensin II on the overflow of tritium evoked by electrical stimulation was checked before and after alpha(2)-adrenoceptor blockade. All the agonists used caused concentration-dependent increases of tritium overflow, the maximal effect representing increases of 44.2, 27.4 and 41.2% for isoprenaline, CGS21680 and angiotensin II, respectively. In the presence of alpha(2)-adrenoceptor blockade by phenoxybenzamine ( 1 microm) or yohimbine (33 or 100 nm), the facilitatory influence of isoprenaline, CGS21680 and angiotensin II was not significantly changed. Since this facilitatory influence, which involves the activation of G(s)- or G(q)-proteins, was not enhanced by alpha(2)-adrenoceptor blockade, it is concluded that the enhancement of the negative modulation resulting from activation of A(1)-adenosine-, muscarine- and kappa -receptors, as previously shown, should be due to the fact that the involved systems share signal transduction mechanisms, or at least G-proteins.
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