Kainic acid lesions of paraventricular nucleus neurons reverse the elevated arterial pressure after aortic baroreceptor denervation in the rat.

The effect of selective destruction of neurons of the paraventricular nucleus of the hypothalamus (PVH) with kainic acid on the maintenance of the elevated arterial pressure (AP) and heart rate (HR) after aortic baroreceptor denervation was investigated in male Wistar rats. The average AP and HR were significantly elevated in two groups of animals which were subjected to bilateral aortic depressor nerve (ADN) transection compared to sham-ADN-transected animals. Microinjections of kainic acid bilaterally into the PVH-reduced the elevated AP and HR in ADN-transected animals to levels which were not significantly different from either sham-ADN-transected animals which received kainic acid injections into the PVH or from predenervation levels. AP and HR in the sham-ADN-transected animals which received bilateral PVH injections of kainic acid were not altered from prelesioned levels. As magnocellular neurons of the PVH have been shown to be resistant to the neurotoxic effects of kainic acid, these data indicate that PVH parvocellular neurons are required for the maintenance of the elevated AP and HR resulting from the removal of aortic baroreceptor inputs to the central nervous system.