The adrenaline-alpha 2-adrenoceptor-mediated vasoconstrictor axis.

In patients with essential hypertension plasma adrenaline concentrations have been found to be higher than in normotensive subjects and this may represent increased adrenergic activity. Adrenaline released into the circulation can be taken up by the sympathetic nerve ending and as it is re-released as a co-transmitter it enhances exocytotic noradrenaline release by stimulating prejunctional beta-adrenoceptors and as a consequence it contributes to postjunctional alpha 1-adrenoceptor-induced vasoconstriction. Adrenaline may also induce vasoconstriction via post- and extra-junctional alpha 2-adrenoceptors, as shown by a decrease in the forearm blood flow during adrenaline infusions in the postjunctional alpha 1- and beta-blocked forearm vasculature, an effect that could be antagonized by alpha 2-adrenoceptor blockade with yohimbine. alpha 2-Adrenoceptor stimulation in platelets showed an increased sensitivity to adrenaline, as determined by sensitivity in counteracting the inhibitor effect of PGI2 on intracellular free calcium concentration in untreated patients with essential hypertension, when compared with treated patients or normotensive subjects. As these effects can be normalized by antihypertensive treatment this suggests that the increased hormone sensitivity may be related to the elevated intracellular free calcium concentration. Thus adrenaline, via pre- and post-junctional adrenoceptors, may contribute to enhanced vascular smooth muscle contraction, which most likely is sensitized by the elevated intracellular calcium concentration.