Excretion of 4-14C-cortisol and l,2-3H-<scp>d</scp>-aldosterone in Human Thermal Sweat1

Jenkins, Melvin E.; Rivarola, Marco A.; Brusilow, Saul W.; Migeon, Claude J.

doi:10.1210/jcem-29-8-1102

Cited by 11 publications

(10 citation statements)

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“…To discount the possibility that part of the aldosterone-2-'H might be excreted in sweat and thereby elevate its secretory rate spuriously by diminishing specific activity of the urinary metabolite, sweat samples were collected during active perspiration into plastic bags sealed over the forearm for several hours after administration of the isotope. These samples were counted in a Packard Tri-Carb, liquid scintillation system (Packard Instrument Co, Downers Grove, Ill. ings of Jenkins, Rivarola, Brusilow, and Migeon (25), it was concluded that significant quantities of tracer were not lost by this route.…”

Section: Methodsmentioning

confidence: 99%

Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Knöchel¹,

Dotin²,

Hamburger³

1972

J. Clin. Invest.

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A B S T R A C T Serial estimations of exchangeable '2Kshowed that six volunteer subjects undergoing intensive physical conditioning in a hot climate sustained a mean deficit of 517 mEq. This deficit occurred despite a daily potassium intake of 100 mEq. Simultaneous values for lean body mass rose suggesting that potassium deficiency was not the result of catabolism. Although sweating was the major avenue by which the deficit occurred, daily excretion of potassium into the urine when each subject was maximally deficient ranged from 46 to 75 mEq and thus was inappropriately high for potassium-depleted subjects. Despite high intakes of sodium and excretion of corresponding quantities' into the urine, Na/K ratios in sweat were low thus indicating unsuppressed activity of aldosterone on sweat glands. Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake.These findings suggest that intense physical work in the heat stimulates higher production of aldosterone than would occur in nonexercising subjects on similar sodium intakes. Similar to the phenomenon of mineralocorticoid escape, such overproduction of aldosterone in the presence of conditions permitting excretion of sodium into the urine could facilitate continued excretion of potassium by the kidney despite serious potassium depletion. As a consequence, the kidney played a role in the genesis of potassium depletion in these subjects.In contrast to subjects undergoing conditioning in the summer months, potassium depletion did not occur in 16Dr. Knochel's present address is The University of Texas (Southwestern) Medical School, Dallas, Tex. and the Veterans Administration Hospital, Dallas, Tex.

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Section: Methodsmentioning

confidence: 99%

Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Knöchel¹,

Dotin²,

Hamburger³

1972

J. Clin. Invest.

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“…Unbound cortisol is thought to diffuse readily into cells due to their lipid-rich cell membrane (Kirschbaum and Hellhammer 1989). This passive transport through lipid bilayer membranes is what likely allows for the detection of cortisol in many bodily fluids in addition to blood, such as saliva (Kirschbaum and Hellhammer 1989;Perogamvros et al 2010;Umeda et al 1981), sweat (Jenkins et al 1969;Jia et al 2016;Lewis and Thorn 1955;Nichols and Miller 1948;Russell et al 2014), and human hair (Raul et al 2004).…”

Section: Cortisolmentioning

confidence: 99%

“…The most compelling study on sweat cortisol mechanisms was published by Jenkins et al (1969), who used an intravenous tracer method to track the movement of cortisol from blood to sweat. In this study, participants received an intravenous infusion of 14 C labeled-cortisol prior to thermally induced sweating.…”

Section: Cortisolmentioning

confidence: 99%

Physiological mechanisms determining eccrine sweat composition

2020

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The purpose of this paper is to review the physiological mechanisms determining eccrine sweat composition to assess the utility of sweat as a proxy for blood or as a potential biomarker of human health or nutritional/physiological status. Methods This narrative review includes the major sweat electrolytes (sodium, chloride, and potassium), other micronutrients (e.g., calcium, magnesium, iron, copper, zinc, vitamins), metabolites (e.g., glucose, lactate, ammonia, urea, bicarbonate, amino acids, ethanol), and other compounds (e.g., cytokines and cortisol). Results Ion membrane transport mechanisms for sodium and chloride are well established, but the mechanisms of secretion and/or reabsorption for most other sweat solutes are still equivocal. Correlations between sweat and blood have not been established for most constituents, with perhaps the exception of ethanol. With respect to sweat diagnostics, it is well accepted that elevated sweat sodium and chloride is a useful screening tool for cystic fibrosis. However, sweat electrolyte concentrations are not predictive of hydration status or sweating rate. Sweat metabolite concentrations are not a reliable biomarker for exercise intensity or other physiological stressors. To date, glucose, cytokine, and cortisol research is too limited to suggest that sweat is a useful surrogate for blood. Conclusion Final sweat composition is not only influenced by extracellular solute concentrations, but also mechanisms of secretion and/or reabsorption, sweat flow rate, byproducts of sweat gland metabolism, skin surface contamination, and sebum secretions, among other factors related to methodology. Future research that accounts for these confounding factors is needed to address the existing gaps in the literature.

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“…Recently, it was reported that chronic stress increases hair cortisol of human and nonhuman primates [8, 25, 26] and that hair cortisol is an effective biomarker for the assessment chronic stress. Blood cortisol diffused in both sebum and sweat, and these may deposit in hair from the outside [7, 13]. In addition, it was demonstrated the existence of a functional HPA-like system in human hair follicles [11].…”

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confidence: 99%

Stress assessment using hair cortisol of kangaroos affected by the lumpy jaw disease

Sotohira

Suzuki

Sano

et al. 2017

The Journal of Veterinary Medical Science

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The aim of this study was to objectively assess stress of kangaroos affected by lumpy jaw disease (LJD) using plasma and hair cortisol concentrations. The plasma and hair samples were collected from kangaroos with LJD and healthy controls. Collected hair samples were extracted with methanol after washing with isopropanol, following which they were processed with the cortisol enzyme immunoassay kit. The plasma cortisol concentration of LJD animals tended to be higher than that of the control. Ventral hair cortisol, but not dorsal hair, of LJD animals was significantly higher than that of the control. In conclusion, stress in kangaroos infected with LJD could be assessed by measuring ventral hair cortisol.

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Excretion of 4-¹⁴C-cortisol and l,2-³H-d-aldosterone in Human Thermal Sweat¹

Cited by 11 publications

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Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Physiological mechanisms determining eccrine sweat composition

Stress assessment using hair cortisol of kangaroos affected by the lumpy jaw disease

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Excretion of 4-14C-cortisol and l,2-3H-d-aldosterone in Human Thermal Sweat1

Cited by 11 publications

References 0 publications

Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Pathophysiology of Intense Physical Conditioning in a Hot Climate. I. MECHANISMS OF POTASSIUM DEPLETION

Physiological mechanisms determining eccrine sweat composition

Stress assessment using hair cortisol of kangaroos affected by the lumpy jaw disease

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Excretion of 4-¹⁴C-cortisol and l,2-³H-d-aldosterone in Human Thermal Sweat¹