Chronically baroreceplor denervated (BD) rats, produced either by selective sino-aortic denervation (SAD) or by electrolytic lesion of the nucleus tractus solitarius (NTS) have normal resting mean arterial pressure (MAP) although the lability of MAP is markedly exaggerated. We have recently demonstrated that the maintenance of resting MAP in BD rats, like baroreceptor intact rats, is dependent upon the integrity of the rostral ventrolateral medulla (RVLM). In baroreceptor intact rats, RVLM neurons involved in cardiovascular control are powerfully inhibited by baroreceptor inputs relayed through the NTS and caudal ventrolateral medulla (CVLM). Acute removal of the tonic baroreceptor-mediated inhibition of the RVLM is responsible for the acute hypertension produced by baroreceptor denervation. The goal of the present study was to determine whether the normal resting MAP in chronic BD rats is accompanied by a restoration of a normal balance between tonic inhibition and excitation of RVLM neurons. Rats were subjected to SAD, NTS lesion, or sham treatment and allowed to recover for approximately 2 weeks. BD rats included in this study had no reflex changes in heart rate to pharmacologically-evoked increases or decreases in MAP. Rats were anesthetized with urethane (1.5 g/kg iv) and prepared for microinjections of drugs into the ventral medulla by either a dorsal approach (SAD) or ventral approach (NTS lesion). Baseline MAP was not different between rats subjected to SAD, NTS lesion, or sham treatment. Microinjection of bicuculline (50 pmol) into the RVLM bilaterally elicited a marked increase in MAP (>40 mm Hg) in all rats, and these responses were not significantly different among the groups. Similarly, inhibition of the CVLM by bilateral injection of muscimol (100 pmol) increased MAP in all rats. These results indicate that in chronic BD rats, the RVLM is inhibited by a GABAergic input under the control of the CVLM. This suggests that the maintenance of normal resting MAP in chronic BD rats is due, at least in part, to a baroreceptor-independent CVLM-medtated inhibition of the RVLM.
|State||Published - 1 Dec 1996|