SUMMARY. The purpose of this study was to examine hemodynamic mechanisms which protect cerebral vessels against chronic hypertension, and contribute to protective effects of sympathetic nerves in the cerebral circulation. We studied stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. At 3-4 weeks of age, all rats underwent removal of one superior cervical sympathetic ganglion. Approximately 1 year later, we cut the superior cervical sympathetic nerve contralateral to the chronic ganglionectomy and exposed pial arterioles on the cerebral cortex ipsilateral or contralateral to the chronic ganglionectomy. We measured aortic, pial arteriolar, and venous pressures with a servo-null technique, and cerebral blood flow with microspheres. Large artery resistance and small vessel resistance were calculated. During control conditions, pressure in pial arterioles was higher in stroke-prone spontaneously hypertensive rats (83 ± 6 mm Hg) (mean ± SE) than in Wistar-Kyoto rats (60 ± 3 mm Hg, P < 0.05), even though large artery resistance was almost two-fold greater in stroke-prone spontaneously hypertensive rats than in Wistar-Kyoto rats (P < 0.05). During maximal dilation produced by seizures, large artery resistance was almost three-fold higher in stroke-prone spontaneously hypertensive rats than in Wistar-Kyoto rats (P < 0.05). Small vessel resistance also was increased in stroke-prone spontaneously hypertensive rats. During seizures in stroke-prone spontaneously hypertensive rats, large artery resistance was 29% lower in chronically denervated vessels than in acutely denervated vessels (P < 0.05). Three stroke-prone spontaneously hypertensive rats had pial vessels with a "sausage string' appearance. Diameter of pial arterioles in the animals with "sausage string" vessels was greater than in stroke-prone spontaneously hypertensive rats with normal vessels (80 ± 1 1 vs. 56 ± 4 ^m, respectively, P < 0.05). We conclude that: first, increases in large artery resistance in stroke-prone spontaneously hypertensive rats attenuate increases in cerebral microcirculatory pressure during chronic hypertension; second, structural changes in cerebral vessels account, in part, for this increased resistance; third, chronic sympathectomy reduces the structural component of resistance of large cerebral arteries in stroke-prone spontaneously hypertensive rats; and, fourth, preliminary evidence suggests that stroke-prone spontaneously hypertensive rats with "sausage string" pial arterioles may have dilation of large cerebral arteries. (CircRes 55: 286-294, 1984)