Effect of hydrostatic pressure on plasma concentrations of norepinephrine during cold water immersion.

Head-out immersion of humans in cold water concurrently stimulates low-pressure receptors and cutaneous cold receptors. In theory, the low-pressure receptors inhibit sympathetic nerve activity to the extent of modifying plasma norepinephrine responses to chilling of the skin. Human plasma norepinephrine concentrations ([NE]p's) were measured when low-pressure receptors were stimulated by 6 h of head-out immersion in thermoneutral water (35 degrees C). The experimental protocol was repeated when cold receptors were activated by a separate exposure to 14.8 degrees C air. Furthermore, both types of receptors were activated by 6 h of immersion in cold water (29.8 degrees C). The control exposure maintained [NE]p close to a constant value of 0.34 ng/ml. Thermoneutral water reduced [NE]p to 0.18 ng/ml after 30 min of immersion, but the change was not statistically significant (two-way ANOVA). [NE]p increased to peak values of 1.5 ng/ml in cold air (P less than 0.05) and 1.1 ng/ml in cold water (P less than 0.5), with no significant differences observed between [NE]p's in cold air and cold water. Equal rates of body heat loss occurred during the exposures to cold air and cold water. Since [NE]p's were comparably raised by separate exposures to cold water and cold air, stimulation of low-pressure receptors by immersion did not significantly depress peripheral vasomotor nerve activity during head-out immersion in cold water.