Abstract

The parvocellular neurons of the paraventricular nucleus (PVN) of the hypothalamus are known to be involved in the control of central autonomic outflow. While the PVN is also known to be involved in the control of fluid-balance, most of the studies examining this nucleus have emphasized the magnocellular neurons, which are involved in the humoral control of fluid-balance and related hemodynamics. The present study took advantage of the differential sensitivity of these two cell types to kainic acid as a means of investigating the role of the parvocellular neurons in the reflex reduction of renal sympathetic nerve discharge (RSND) during acute isotonic volume expansion. Kainic acid (18 pmol), which destroys parvocellular but not magnocellular neurons in the PVN, was microinjected (20 nl) bilaterally at sites in and adjacent to the PVN 3–4 days prior to acute isotonic volume expansion. In anesthetized rats RSND decreased by 59% at the completion of acute isotonic volume expansion (10% of body weight) in the vehicle-injected control group; on the other hand, it decreased by 33% in the kainic acid-treated group. The effect of destruction of the parvocellular neurons on the baroreceptor reflex was also examined. Neither the renal nerve component (Δ%RSND/ΔAP), nor the heart rate component (ΔHR/ΔAP), of the baroreceptor reflex were different in the kainic acid-treated group (3.1 ± 0.4, and 1.1 ± 0.1, respectively) than in the vehicle-injected control group (2.9 ± 0.7, and 0.8 ± 0.1, respectively). We conclude that the parvocellular neurons of the PVN are an important synaptic relay site in the reflex arc that is activated during isotonic volume expansion, but not in the baroreceptor reflex.

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