ROLE OF VAGAL NERVES AND ATRIAL NATRIURETIC HORMONE IN VASOPRESSIN RELEASE AND A DIURESIS UNDER HYPERTONIC VOLUME EXPANSION

To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume r eceptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volu me expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran ( 9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/I NaCl alone was administered. Plasma AVP and ANH and cardio vascular and renal functions were determined. Hypertonic saline and 9D -HS also were administered into the vagotomized and sham operated dogs , and the same parameters were determined. Mean blood pressure and hea rt rate never changed in all the groups, but central venous pressure a nd plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increase d slightly but plasma volume never changed. Plasma AVP increased in th e order of hypertonic saline, 6D-HS and 9D-HS, but plasma ANH increase d in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma AN H. Urine sodium and potassium excretion and urine flow increased in hy pertonic saline, 6D-HS and 9D-HS groups, but these increases were comp arable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an e ffect on the suppression of the AVP response to osmotic stimuli, and i ncreased plasma ANH release never potentiated the natriuresis under th e hypertonic plasma volume expansion.