Previous findings suggest that chronic ANG II hypertension is neurally mediated while acute ANG II hypertension results from direct action on the vasculature. Transition from a peripheral to a neural effect occurs after about 10 hr of ANG II infusion in rats. Using immunocytochemlstry (polyclonal sheep antibody from Cambrige Res. Biochem.; DAB peroxidase method), the FLI, indicting neural activity, was measured in the caudal ventrolateral medulla (cVLM) and the rostral ventrolateral medulla (rVLM) of adult rats after acute ANG II (10 μl/min. i.v., 2 hr), chronic ANG II (1 μl/hr i.v., 18 hr) or vehicle (5% dextrose 10 μl/min i.v., 2 hr) infusions. Acute and chronic ANG II infusion (50 ng/kg/min) produced comparable increases in arterial pressure. Acute ANG II infusion increased FLI in the cVLM (62%) and in the rVLM (34%) compared to the controls. In contrast, chronic ANG II infusion did not change FLI in the cVLM but increased FLI in the rVLM compared to both vehicle (110%) and acute ANG II (57%) infusion. The cVLM, a region associated with sympathoinhibition, is activated during acute ANG II infusion whereas the rVLM, a brain site associated with sympathoexdtation, is activated by chronic ANG II infusion. Activation of the cVLM by acute ANG II may be due to baroreflex activation and is consistent with ANG II acting at peripheral sites. Activation of the rVLM by chronic ANG II is consistant with a centrally-mediated increase in sympathetic outflow related to a transition from a peripheral to a central site of action for chronic ANG II.
|State||Published - 1 Dec 1996|