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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 less than 0.05), even though large artery resistance was almost two-fold greater in stroke-prone spontaneously hypertensive rats than in Wistar-Kyoto rats (P less than 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 less than 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 less than 0.05). Three stroke-prone spontaneously hypertensive rats had pial vessels with a "sausage string" appearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chronic hypertension and sympathetic nerves on the cerebral microvasculature of stroke-prone spontaneously hypertensive rats.