BODY-TEMPERATURE MODIFICATION OF OSMOTICALLY INDUCED VASOPRESSIN SECRETION AND THIRST IN HUMANS

We examined the effect of increased body core temperature (T-es) on th e plasma arginine vasopressin concentration ([AVP](p)) and thirst resp onses to increased plasma osmolality (P-osm) induced by 3% NaCl infusi on for 120 min in seven healthy humans. T-es was increased by immersio n of the lower legs in 41 degrees C water in a 28 degrees C room (pass ive heating; HT). Immersion of the lower legs in 34.5 degrees C water on a separate day served as the control (thermoneutral; NT). The 120-m in hypertonic saline infusion was initiated 30 min after the onset of leg immersion and was followed by a 30-min rehydration period. T-es in HT increased by 0.21 +/- 0.04 degrees C before infusion and by 0.86 /- 0.08 degrees C at the end of infusion. The change in T-es in NT bef ore and after the infusion was negligible. P-osm was increased by 15.0 +/- 1.0 mosmol/kgH(2)O by infusion in both NT and HT. [AVP](p) increa sed by 3.48 +/- 0.72 pg/ml in NT and by 7.59 +/- 1.02 pg/ml in HT. Thu s the increase in [AVP](p) at a given increase in P-osm was markedly h igher in HT than in NT. The plasma renin activity response to hyperton ic saline infusion in both conditions was similar. Subjective thirst r ating and cumulative water intake during rehydration were higher in HT than in NT. The calculated increase in [AVP](p) per unit rise in T-es at a P-osm of 299 +/- 1 mosmol/kgH(2)O was 4.23 +/- 0.85 pg . ml(-1). degrees C-1, significantly higher than the 1.68 +/- 1.10 pg . ml(-1).d egrees C-1 increase at a P-osm of 284 +/- 1 mosmol/kgH(2)O. Our data i ndicate that the effect of increased T-es and P-osm on [AVP](p) is not simply additive but P-osm dependent. We conclude that increased T-es modulates osmotically induced AVP secretion in a P-osm-dependent manne r.