Influence of chemoreceptors on neurohypophyseal blood flow during hypoxic hypoxia

Neurohypophyseal blood flow was studied using radiolabelled microspheres in 13 dogs. Hypoxic hypoxia and carbon monoxide hypoxia with similar arterial oxygen contents (CaO2, approximately 8 vol %) were produced. Under conditions of hypoxic hypoxia, 100-200% increases in blood flow in caudate nucleus, white matter, neurohypophysis, and all other brain regions occurred. Similar blood flow responses were observed with carbon monoxide hypoxia in all brain regions except the neurohypophysis. The role of carotid and aortic chemoreceptors in mediating this blood flow response was studied in 6 additional dogs. Similar degrees of hypoxic hypoxia were produced in chemoreceptor-intact and completely denervated animals (CaO2 approximately 8 vol %, PaO2 approximately 33 mm Hg). Hypoxic hypoxia produced a 250% increase in neurohypophyseal blood flow and a concurrent rise in plasma arginine vasopressin from 8 +/- 3 to 52 +/- 8 pg/ml. Chemoreceptor denervation completely inhibited the increase in neurohypophyseal blood flow associated with hypoxic hypoxia. Arginine vasopressin was not increased by hypoxic hypoxia under conditions of complete denervation. A unique role for peripheral chemoreceptors in regulating neurohypophyseal blood flow is postulated.