α2 Adrenoceptor-mediated vasoconstriction of arteries

We investigated the possibility that adrenoceptors of the alpha 2 subtype mediate vasoconstriction of arteries in response to administered catecholamines. Clonidine, which in vitro, stimulates alpha 2-adrenoceptors was infused into a brachial artery in 12 subjects (0.48 micrograms/min/100 ml tissue for 3 min). Afterward, prazosin was infused intraarterially in the first six subjects (0.5 micrograms/min/100 ml for 10 min) and in the remaining subjects, phentolamine was infused (0.12 micrograms/min/100 ml) for 10 min. Subsequently, the clonidine infusion was repeated. Clonidine decreased forearm blood flow from 3.5 +/- 0.52 to 1.8 +/- 0.32 in the first six subjects and from 4.2 +/- 0.84 to 2.7 +/- 0.61 ml/min/100 ml in the other subjects. Alpha 1-Adrenoceptor blockade by prazosin increased forearm blood flow by 122.7 +/- 33.8% and combined alpha 1 and alpha 2 blockade by phentolamine by 127.2 +/- 29.9%, indicating much the same degree of postjunctional alpha-adrenoceptor blockade. Alpha 2-Adrenoceptor-mediated vasoconstriction by clonidine was abolished after phentolamine (9.1 +/- 2.29 and 9 +/- 2.51 ml/min/100 ml) but was still present after prazosin (7.8 +/- 1.7 and 4.8 +/- 1.6 ml/min/100 ml). The results suggest that, apart from the classical alpha 1 adrenoceptor, there is a second type of adrenergic receptor on smooth muscle cells that can mediate vasoconstriction, resembling the alpha 2-adrenoceptor pharmacologically.