Abstract
Passive or neurogenic hypertension was produced by ligation of the aorta or microinjection of glutamate diethyl ester (GDEE) into the intermediate one-third of the nucleus tractus solitarius (NTS), respectively, in 44 anesthetized, artificially ventilated rats. After bilateral sympathectomy, the blood flow (microsphere method) was increased in the cerebral cortex, thalamus, and mesencephalon in a pressure-dependent manner in the face of neurogenic hypertension, as compared with the flow during passive hypertension. We speculate that some neurogenic mechanism tends to impair cerebrovascular autoregulation when afferents arising from cardiovascular receptors were blocked by GDEE within the NTS.
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