AJP - Endocrinology and Metabolism, Vol 243, Issue 6 522-E526, Copyright © 1982 by American Physiological Society
Effect of hypertonic intracarotid infusions on plasma vasopressin concentration
C. E. Wade, P. Bie, L. C. Keil and D. J. Ramsay
The effect of short-term bilateral intracarotid infusions of hypertonic
saline on plasma vasopressin concentration (pAVP) was evaluated in five
dogs. Intracarotid infusion of saline at 90 mumol . kg-1 . min-1 . artery-1
significantly (P less than 0.05) increased jugular vein osmolality (pOsm)
and sodium concentration (pNa+) within 2 min. Saphenous vein pOsm was not
altered during the 6 min of infusion, whereas pNa+ was increased (P less
than 0.05) from 0.8 +/- 0.1 to 2.3 +/- 0.3 pg/ml. Subsequent experiments
using hypertonic saline infusions of 90 and 180 mumol . kg-1 . min-1
administered intracarotidly and intravenously for 6 min were performed.
Intracarotid isotonic infusions and intravenous hypertonic infusions did
not significantly alter pAVP. Hypertonic intracarotid saline increased
jugular vein pOsm and pNa+ in a dose-related fashion, whereas saphenous
vein pOsm and pNa+ were not significantly changed after 6 min of infusion.
Plasma vasopressin, compared with the isotonic intracarotid infusion (1.5
+/- 0.3 pg/ml), was increased (P less than 0.05) after hypertonic saline to
3.2 +/- 0.6 and 4.8 +/- 0.2 pg/ml for the 90 and 180 mumol . kg-1 . min-1
infusions, respectively. The cerebral osmolality indicated by jugular vein
pOsm was therefore increased in the absence of changes in systemic pOsm
during intracarotid hypertonic infusions. The increase in pAVP in response
to these changes in pOsm supports the presence of central osmoreceptors
regulating vasopressin release in the area of distribution of the common
carotid arteries.
