This paper attempts to further clarify the characteristics of Mecholyl- or epinephrine-stimulated glucose metabolism in the isolated monkey eccrine sweat gland with special emphasis on its relationship to increased sodium transport. The Mecholyl- or epinephrine-stimulated glucose metabolism (as estimated by either lactate or 14CO2 production or both) is seen only in the secretory coil and not in the duct. It is markedly suppressed in the absence of glucose, Na+, or K+. It is inhibited by ouabain (10−3 M) and partially suppressed in a low-sodium (40 mM), high-potassium (100 mM) medium.
2,4-dinitrophenol (10−4 M) reverses ouabain-induced inhibition of lactate and 14CO2 production but only partially reverses inhibition induced by Na+ + K+ deprivation, indicating that metabolic inhibition by ouabain is secondary to the inhibition of sodium transport. There is no synergism between Mecholyl and epinephrine. The absence of any significant inhibitory effects by acetazolamide (Diamox) or HCO3−-free media suggests that H+ transport may not be important in sweat gland function. In contrast to a report by Wolfe et al., human eccrine sweat glands show considerable oxidative activity (14CO2 production of 0.42-0.72 nmol/gland/h). These observations are discussed in terms of the linkage between sweat gland energy metabolism and sodium transport.