LESIONS IN ROSTRAL VENTROMEDIAL OR ROSTRAL VENTROLATERAL MEDULLA BLOCK NEUROGENIC HYPERTENSION

Neurogenic hypertension results from the removal of inhibitory barorec eptor afferent input to vasomotor systems in the central nervous syste m. We sought to determine whether the bilateral destruction of neurons in the rostral ventrolateral or rostral ventromedial medulla, made us ing microinjections of N-methyl-D-aspartic acid (30 nmol in 200 nL), w ould block the acute increase in arterial pressure after sinoaortic de afferentation in pentobarbital-anesthetized rats. Bilateral lesions of the rostral ventrolateral or rostral ventromedial medulla decreased m ean arterial pressure (107+/-4 to 78+/-5 and 115+/-3 to 94+/-3 mm Hg, respectively). In rostral ventrolateral or rostral ventromedial medull a lesioned rats, sinoaortic deafferentation failed to increase arteria l pressure. Sham lesions or lesions placed rostral to the rostral vent rolateral or rostral ventromedial medulla did not significantly lower arterial pressure. Subsequent sinoaortic deafferentation significantly increased mean arterial pressure (109+/-3 to 145+/-4 and 109+/-5 to 1 41+/-3 mm Hg, respectively). In eight rats we used an infusion of angi otensin II to return arterial pressure to control levels after lesion of the rostral ventrolateral (n=4) or rostral ventromedial (n=4) medul la. In these animals, sinoaortic deafferentation failed to increase ar terial pressure. We conclude that neurons in the rostral ventrolateral and rostral ventromedial medulla are involved in the normal maintenan ce of arterial pressure and the development of hypertension after sino aortic deafferentation in pentobarbital-anesthetized rats.