α₂‐Adrenoceptor agonists potentiate responses mediated by α₁‐adrenoceptors in the cat nictitating membrane

α2‐Adrenoceptor agonists enhance vasoconstrictor responses to α1‐adrenoceptor agonists in the rat tail artery by increasing the influx of Ca2+

“…(1987a) and Xiao & Rand (1989a), using the same preparation, that vasoconstrictor responses to a1-adrenoceptor agonists are markedly enhanced by a2-adrenoceptor agonists in concentrations that are one-hundredth to one-thousandth of the concentrations producing other prejunctional or postjunctional effects. Similar observations were made by Shepperson (1984), who found that UK14304 in doses producing only small contractions of the cat nictitating membrane markedly enhanced contractile responses to phenylephrine. The enhancing effect of TL99 on vasoconstrictor responses to noradrenaline was abolished by the relatively selective M2-adrenoceptor antagonist idazoxan (Doxey et al, 1983), confirming our previous findings that idazoxan blocked the enhancement by a2-adrenoceptor agonists of responses resulting from activation of al-adrenoceptors by sympathetic nerve stimulation (Xiao et al, 1987a;Xiao & Rand, 1989a) and responses elicited by certain other vasoconstrictor agents (unpublished observations).…”

“…We have previously suggested that the function of postjunctional a2-adrenoceptors may be to augment the stimulus produced by activation of a,-adrenoceptors (Xiao & Rand, 1989a). A similar suggestion has been made by Shepperson (1984) on the basis of experiments with the cat nictitating membrane. Such an ancillary role for postjunctional x2-adrenoceptors might account for the functional interaction between a-adrenoceptor subtypes observed by Daly et al (1988) in isolated vascular preparations, and for the suggestion by Sulpizio & Hieble (1987) that a circulating factor was necessary for the expression of pressor responses to a2-adrenoceptor agonists in vivo.…”

Postjunctional α‐adrenoceptors in the rabbit isolated distal saphenous artery: indirect sensitivity to prazosin of responses to noradrenaline mediated via postjunctional α2‐adrenoceptors

“…Again in this preparation, the facilitatory action of AII on postjunctional a2-adrenoceptor-mediated responses is apparent only if al-adrenoceptors are blocked by prazosin or phenozybenzamine (Dunn et al, 1991). An even more subtle interaction between al-and X2-adrenoceptors has been demonstrated in the cat nictitating membrane (Shepperson, 1984) and rat isolated tail artery (Xiao & Rand, 1989 Since the original demonstration of postjunctional a2-adrenoceptors in the pithed rat (Drew & Whiting, 1979;Docherty et al, 1979), identification of this subtype in isolated vascular preparations, both responding to NA and resistant to prazosin or a suitable xl-adrenoceptor antagonist, has proved very difficult. While a number of explanations have been put forward to explain the elusive nature of this receptor subtype (see McGrath et al, 1989), it is clear from the present study that one such factor that may conspire to render contractions mediated by postjunctional a2-adrenoceptors 'prazosinsensitive', is the dependency of a2-adrenoceptor-mediated contractions on stimulation of ax-adrenoceptors.…”

Pharmacological analysis of postjunctional α‐adrenoceptors mediating contractions to (−)‐noradrenaline in the rabbit isolated lateral saphenous vein can be explained by interacting responses to simultaneous activation of α1‐and α2‐adrenoceptors

“…The appearance of the rauwolscine-resistant component to NA was also observed in the absence of both cocaine and propranolol or in the presence of the neuronal uptake inhibitor desipramine, thus eliminating the possibility that this is due to an effect of the ancillary drugs used to optimize the condi- tions for the study of the a-adrenoceptors (see Schumann & Lues, 1983). The appearance of a 'rauwolscine-resistant' response to NA could conceivably be a consequence of the transient contractile response to rauwolscine reducing the threshold for contraction (see: Stupecky et al, 1986), but this seems unlikely since CH-38083 failed to elicit similar responses while corynanthine (50 SIM) and phentolamine caused transient contractions without effecting a change in the slope of the NA CRC. Furthermore, transient contractions produced by prazosin in the rabbit isolated aorta (Cavero et al, 1978) and yohimbine in the rabbit isolated ear artery (Tayo, 1982) were not associated with the appearance of a resistant component to NA.…”

“…The authors suggested that this was indicative of a functional interaction between two subtypes of adrenoceptor that mediate the same response. Similarly, Shepperson (1984) has demonstrated an even more subtle interaction between a functionally active population of a,-adrenoceptors and a 'quiescent' population of a2-adrenoceptors on the cat nictitating membrane. Contractile responses to selective ac-adrenoceptor agonists were potentiated by prior exposure to a selective a2-adrenoceptor agonist even though these agonists failed to elicit a functional response, and this effect was inhibited by selective X2-adrenoceptor antagonists.…”