Electrical stimulation of the rostral fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rats with a 10-s stimulus train elicited a stimulus-locked elevation of arterial pressure (AP) and heart rate (HR) (the fastigial pressor response, FPR) and elevated plasma catecholamines (CA) within 20 s from the onset of stimulus. Norepinephrine (NE) increased from 139 ± 24 to 280 ± 43 pg/ml (P < 0.05, n = 8) and epinephrine (E) from 70 to 26 to 360 ± 107 pg/ml (P < 0.02, n = 8). Acute adrenalectomy increased basal plasma NE (362 ± 108 pg/ml, P < 0.05, n = 6) and reduced E (9 ± 4 pg/ml, P < 0.02, n = 6). The magnitude and duration of the FPR and the relative increase of NE were unchanged; however, the elevation of E was abolished. Chemosympathectomy, produced by 6-hydroxydopamine hydrobromide (100 mg/kg iv, 24 h before the experiment), lowered resting AP (from 122 ± 2 to 77 ± 1 mmHg, P < 0.001) and NE (16 ± 5 pg/ml, P < 0.01), but not E. After chemosympathectomy, FN stimulation induced a pressor response of greater magnitude and longer latency and duration than in controls, increased NE 3.5-fold (from 16 ± 5 to 56 ± 14 pg/ml, P < 0.05, n = 5) and E 9-fold (from 38 ± 11 to 336 ± 88, P < 0.05, n = 5). The increases in CA were abolished by adrenalectomy. Chemosympathectomy shifted the pressor-dose-response curves of NE and E to the left; thus, the enhanced pressor response to FN stimulation after chemosympathectomy was possibly a consequence of supersensitivity to circulatory CA. Stimulation of cerebellar FN increased plasma CA, as a consequence of coexcitation of both neural and adrenomedullary components of the autonomic nervous system. However, in rats with intact sympathetic nerves the release of adrenomedullary CA did not contribute to the elevation in AP.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1983|
ASJC Scopus subject areas
- Physiology (medical)