Vasopressin secretion by hypertonic saline infusion during hemodialysis: effect of cardiopulmonary recirculation.

Intradialytic hypotension is the most common and severe acute complication of hemodialysis therapy. In our previous study, infusion of 20 mL of 10% saline into the venous line of a dialyzer increased blood pressure during dialysis hypotension by stimulating arginine vasopressin (AVP) secretion, independent of its effect on plasma volume (PV). This study examines the mechanism by which a small amount of hypertonic solution stimulates AVP secretion. Hemodialysis patients were infused with 20 mL of 2.5 M saline (100 mOsm) over 5 (Protocol 1) or 2 min (Protocol 2) or with isotonic saline (Protocol 3) into the venous line. Arterial plasma osmolality (Posm) increased by 28.1 and 16.0 (P < 0.0001), while peripheral venous Posm increased by only 8.6 and 8.9 mOsm/kg H2O (P < 0.001) in Protocols 2 and 1, respectively. Plasma AVP (P-AVP) increased significantly by 18.6 and 5.6 pg/mL, PV by 7.2 and 5.5% and mean arterial pressure (MAP) by 15.0 and 7.2 mmHg in Protocols 2 and 1, respectively. Thus, there were large differences in Posm between arterial and peripheral venous blood; osmolar gap, P-AVP and MAP increased in proportion to the infusion rate. Isotonic saline (30.8 mOsm) infusion increased PV by 8.7% and MAP by 7.2 mmHg. Our results indicate that by a mechanism similar to cardiopulmonary recirculation, hypertonic saline infusion caused a striking increase in arterial Posm that enhanced AVP secretion and raised blood pressure. The effect of hypertonic saline on PV was less than one-third of isotonic saline under similar osmolar loads.