Adrenaline induces vasoconstriction through post-junctional alpha 2 adrenoceptors and this response is enhanced in patients with essential hypertension.

The role of adrenaline-induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction was studied in seven patients with essential hypertension (EHT) and eight normotensive subjects (NT) using forearm venous occlusion plethysmography. Adrenaline (0.01 to 0.08 micrograms/min/100 ml of tissue) infused into the forearm circulation via the brachial artery during alpha l adrenoceptor blockade with prazosin (0.05 micrograms/min/100 ml of tissue) and beta adrenoceptor blockade with propranolol (2 micrograms/min/100 ml of tissue) decreased forearm blood flow (FAF) dose-dependently below basal FAF (P less than 0.001). The adrenaline-induced decrease in FAF was greater in EHT than in NT (P less than 0.01) and was blocked in both groups by alpha 2 adrenoceptor blockade with yohimbine (30 micrograms/min/100 ml of tissue). The increase in FAF following postjunctional alpha-2 blockade as well as following postjunctional alpha-1 blockade was greater in EHT than in NT (P less than 0.01) but was similar in both groups following 'non-specific' vasodilation with sodium nitroprusside. Postjunctional alpha 1 and alpha 2 adrenoceptor-mediated vasoconstriction is enhanced in patients with essential hypertension. Adrenaline induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction could contribute to elevated vascular resistance in patients with EHT and elevated plasma adrenaline concentrations particularly in the presence of blunted beta adrenoceptor-mediated functions.