Lack of interaction between α2-autoreceptors and prejunctional receptors mediating a facilitatory effect on noradrenaline release

Release inhibitory receptors activation favours the A2A‐adenosine receptor‐mediated facilitation of noradrenaline release in isolated rat tail artery

“…However, in the present experimental conditions, the selective A 2A ‐receptor agonist CGS 21680 enhanced noradrenaline release only when α 2 ‐autoinhibition was occurring: blockade of α 2 ‐autoreceptors with yohimbine prevented the A 2A ‐mediated facilitation of noradrenaline release caused by CGS 21680. This observation is in agreement with results published recently (Mota et al ., 2000). An A 2A ‐receptor‐mediated facilitation was previously observed even in the presence of yohimbine (Gonçalves & Queiroz, 1996).…”

“…The present study confirms previous observations (Gonçalves & Queiroz, 1996; Mota et al ., 2000) indicating the presence of release‐facilitatory A 2A ‐adenosine receptors in the rat tail artery. However, in the present experimental conditions, the selective A 2A ‐receptor agonist CGS 21680 enhanced noradrenaline release only when α 2 ‐autoinhibition was occurring: blockade of α 2 ‐autoreceptors with yohimbine prevented the A 2A ‐mediated facilitation of noradrenaline release caused by CGS 21680.…”

“…The release‐facilitatory effect of angiotensin II was reported to be increased (Costa & Majewski, 1988), decreased (Cox et al ., 2000) or not influenced (Mota et al ., 2000) by blockade of α 2 ‐autoreceptors. Furthermore, it was also reported that the release‐facilitatory effect mediated by β‐adrenoceptors was increased (Majewski & Rand, 1981; Johnston & Majewski, 1986) or not influenced (Cox et al ., 2000; Mota et al ., 2000) by blockade of α 2 ‐autoreceptors. The reasons for these differences are not understood but may be the use of different tissue preparations and/or different stimulation parameters.…”

Crosstalk between presynaptic angiotensin receptors, bradykinin receptors and α2‐autoreceptors in sympathetic neurons: a study in α2‐adrenoceptor‐deficient mice

“…We have also extended the evidence that stimulation of the presynaptic G i/o inhibitory pathway through other receptors, namely neuropeptide Y Y 2 ‐, opioid OP 1 ‐ and–this is the new finding–cannabinoid CB 1 ‐receptors can replace G i/o stimulation through α 2 ‐autoreceptors to permit full presynaptic facilitation by angiotensin II and bradykinin. The results should not be interpreted as indicating that interruption of α 2 ‐autoinhibition is the sole presynaptic mode of action of angiotensin II and bradykinin; there may be α 2 ‐autoinhibition‐independent mechanisms (see Costa & Majewki, 1988; Mota et al ., 2000); indeed, small facilitatory effects of the two peptides in the presence of phentolamine plus rauwolscine or during brief high‐frequency stimulation were occasionally seen throughout the present work (e.g. Figure 1 and Figure 8); however, in the preparations examined the interruption of autoinhibition prevailed.…”