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Many investigators have demonstrated that sympathetic sudomotor activity sufficient to cause visible sweating is accompanied by a decrease in electrical skin resistance (ESR). Furthermore, the reciprocal of resistance (conductance) was shown to be linearly related to the amount of perspiration and the number of visibly active sweat glands. The present study examines the relationship of ESR to sweat-gland activation under apparently nonsweating circumstances, and clarifies the significance of topographical differences in ESR observed in human studies conducted at moderate (nonsweating) temperatures; results also suggest a neural influence on insensible perspiration. Comparisons in adjacent high- and low-resistance areas were made of the sweat gland responses produced by intradermal injections of drugs that directly stimulate sweat glands. When just-threshold quantities of acetylcholine (ACh), pilocarpine, or epinephrine were used, the low-resistance areas always responded with more numerous activated glands. When both high- and low-resistance areas were injected with procaine approximately 10 min prior to ACh injection, activated sweat gland response was essentially similar in both areas. At moderate temperatures, sweat glands evidently receive sudomotor impulses at a rate that does not produce visible sweating, but does increase transcutaneous water transfer and electrolyte conductance Submitted on February 21, 1961

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