Sympathetic activation and contribution of genetic factors in hypertensionwith neurovascular compression of the rostral ventrolateral medulla

Objective The rostral ventrolateral medulla is an important center for the regulation of sympathetic and cardiovascular activities. Reportedly, neurov ascular compression of the rostral ventrolateral medulla may be causally re lated to essential hypertension. We aimed to determine the mechanism behind elevated blood pressure in hypertensive patients with compression of the r ostral ventrolateral medulla and to investigate whether genetic factors con tribute to the etiology of hypertension with compression. Design and methods The study included 56 patients with essential hypertensi on and 25 normotensive individuals. With the use of magnetic resonance imag ing, the essential hypertension group was subdivided into hypertension with compression and without compression groups. We compared plasma levels of h ormones that raise blood pressure and family histories of hypertension betw een the two hypertension groups and the normotension group. Results Plasma norepinephrine levels, but not plasma renin activity, aldost erone, epinephrine, or vasopressin levels, were significantly higher in the hypertension with compression group (389 +/- 53 pg/ml) than in the hyperte nsion without compression group (217 +/- 38, P < 0.05) or in the normotensi on group (225 +/- 30, P < 0.05), The percentage of individuals who had two hypertensive parents was significantly higher in the hypertension with comp ression group (39.4%) than in the hypertension without compression group (1 3.0%, P < 0.05) or in the normotension group (8.0%, P < 0.01). Conclusions These results indicate that neurovascular compression of the ro stral ventrolateral medulla might be, at least in part, causally related to essential hypertension by increasing sympathetic nerve activity, They also suggest that genetic factors might contribute to the etiology of hypertens ion with neurovascular compression. (C) Lippincott Williams & Wilkins.