ALTERED C-FOS IN ROSTRAL MEDULLA AND SPINAL-CORD OF SPONTANEOUSLY HYPERTENSIVE RATS

Neurons immunoreactive for Fos, the protein product of the immediate e arly gene c-fos, have been compared in the rostral ventral medulla and spinal. cord of conscious normotensive Wistar-Kyoto rats (WKY) and sp ontaneously hypertensive rats (SHR) after baroreceptor unloading. Hypo tension induced by a 60-minute intravenous infusion of sodium nitropru sside reduced baroreceptor activity; controls received intravenous sal ine. In WKY, 474+/-56 (n=6) Fos-positive neurons were identified in th e rostral ventral medulla after nitroprusside infusion, a fivefold inc rease from controls; 50% of the tyrosine hydroxylase-containing neuron s in the rostral ventral medulla were activated by this hypotension. S ympathetic preganglionic neurons, mainly sympathoadrenal neurons, were Fos positive after nitroprusside, but Fos-positive sympathetic pregan glionic neurons were not observed in control WKY. In SHR, Fos immunore activity in the rostral ventral medulla was elevated in the control gr oup compared with the WKY controls (236+/-31 and 93+/-15, respectively , n=6 for both). Nitroprusside hypotension did not further increase Fo s immunoreactivity in the rostral ventral medulla, although the number of Fos-positive spinal sympathetic neurons increased. Our results hav e identified different neuronal activities between WKY and SHR in site s that are critical to sympathetic outflow. In WKY, nitroprusside effe cts are consistent with an activation of rostral ventral medulla neuro ns, including bulbospinal neurons, that are normally inhibited by baro receptor activity. In SHR, basal nerve activity is increased, so even at rest, rostral ventral medulla neurons and sympathetic preganglionic neurons, mainly sympathoadrenal neurons, are Fos immunoreactive. Thes e activated neurons are likely to contribute to the elevated blood pre ssure in this rat strain.