Peripheral chemoreceptor control of neurohypophysial blood flow

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O₂ tension was lowered from 128 ± 3 to 31 ± 1 Torr, whereas pH and arterial CO₂ tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from ~8 to ~40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.