Osmoregulatory inhibition of thermally induced cutaneous vasodilation in passively heated humans.

We examined the effect of increased plasma osmolality (P(osm)) on cutaneous vasodilatory response to increased esophageal temperature (T(es)) in passively heated human subjects (n = 6). To modify P(osm), subjects were infused with 0.9, 2, or 3% NaCl infusions (Inf) for 90 min on separate days. Infusion rates were 0.2, 0.15, and 0.125 ml.min-1.kg body wt-1 for 0.9, 2, and 3% Inf, respectively, which produced relatively similar plasma volume expansion. Thirty minutes after the end of infusion, subjects immersed their lower legs in a water bath at 42 degrees C (room temperature 28 degrees C) for 60 min after 10 min of preheating control measurements. Passive heating without infusion (NI) served as time control to account for the effect of volume expansion. P(osm) (mosmol/kgH2O) values at the onset of passive heating were 289.9 +/- 1.4, 292.1 +/- 0.6, 298.7 +/- 0.7, and 305.6 +/- 0.6 after NI, 0.9% Inf, 2% Inf, and 3% Inf, respectively. The increases in T(es) (delta T(es)) at equilibrium during passive heating (mean delta T(es) during 55-60 min) were 0.47 +/- 0.08, 0.59 +/- 0.08, 0.85 +/- 0.13, and 1.09 +/- 0.12 degrees C after NI, 0.9% Inf, 2% Inf, and 3% Inf, respectively, which indicates that T(es) at equilibrium increased linearly as P(osm) increased. delta T(es) required to elicit cutaneous vasodilation (delta T(es) threshold for cutaneous vasodilation) also increased linearly as P(osm) increased as well as the delta T(es) threshold for sweating. The calculated increases in these thresholds per unit rise in P(osm) from regression analysis were 0.044 degree C for the cutaneous vasodilation and 0.034 degree C for sweating. Thus the delta T(es) thresholds for cutaneous vasodilation and sweating are shifted to higher delta T(es) along with the increase in P(osm), and these shifts resulted in the higher increase in T(es) during passive heating.