An elevated sympathoadrenal tone and an imbalance in postsynaptic alpha- and beta-
adrenoceptor function are discussed as factors in the pathogenesis of
essential hypertension. This study examined plasma
catecholamines, thrombocyte alpha2-adrenoceptors and lymphocyte beta2-adrenoceptors in 16 young patients with newly detected
essential hypertension and 26 normotensive age matched controls (27.1 +/- 4.5 vs. 24.8 +/- 2.8 years; NS). Plasma
noradrenaline (276 +/- 34 vs. 216 +/- 18 pg/ml, P < 0.05) and plasma
adrenaline (96 +/- 15 vs. 31 +/- 4 pg/ml, P < 0.0001) were significantly elevated in hypertensive patients. Thrombocyte alpha2-adrenoceptor density was only nonsignificantly decreased (230 +/- 37 vs. 311 +/- 36 fmol/mg
protein, NS), whereas lymphocyte beta2-adrenoceptor density was markedly reduced (15.3 +/- 2.3 vs. 22.6 +/- 1.8 fmol/mg
protein, P < 0.01) in hypertensive patients. Elevated plasma
catecholamines are consistent with a pathophysiological role for increased sympathetic neural activity in young hypertensive patients. Assuming that results of
adrenoceptor studies on blood elements are applicable on vascular receptors, our results are consistent with an imbalance of postsynaptic
adrenoceptor functions which promotes the pressor effects of the sympathetic system.