Antidiuretic hormone and human eccrine sweating.

Fasciolo, J. C.; Totel, G. L.; Johnson, Robert E.

doi:10.1152/jappl.1969.27.3.303

Cited by 32 publications

(12 citation statements)

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“…The presence of AVP receptors within human sweat glands is only weakly supported by indirect evidence (37). Prior investigations looking specifically at the effects of vasoconstriction on sweat rate and composition do not support activation of the V1aR as a plausible mechanism for any association between sweat [Na ϩ ] and [AVP] P (7,33,34,45). Therefore, AVP-mediated insertion of AQP5 water channels through activation of the V2R within the apical membrane of the sweat gland remains an enticing, yet unexplored, mechanism.…”

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confidence: 99%

Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise

Hew‐Butler

Hummel

Rider

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Hew-Butler T, Hummel J, Rider BC, Verbalis JG. Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise. Am J Physiol Regul Integr Comp Physiol 307: R366 -R375, 2014. First published June 18, 2014 doi:10.1152/ajpregu.00120.2014.-A regulatory effect of arginine vasopressin (AVP) on sweat water conservation has been hypothesized but not definitively evaluated. AVP-mediated insertion of sweat and salivary gland aquaporin-5 (AQP5) water channels through activation of the vasopressin type 2 receptor (V2R) remains an attractive, yet unexplored, mechanism that could result in a more concentrated sweat with resultant decreased water loss. Ten runners participated in a double-blind randomized control treadmill trial under three separate pharmacological conditions: a placebo, V2R agonist (0.2 mg desmopressin), or V2R antagonist (30 mg tolvaptan). After a familiarization trial, runners ran for 60 min at 60% of peak speed followed by a performance trial to volitional exhaustion. Outcome variables were collected at three exercise time points: baseline, after the steady-state run, and after the performance run. Body weight losses were Ͻ2% across all three trials. Significant pharmacological condition effects were noted for urine osmolality [F ϭ 84.98; P Ͻ 0.0001] and urine sodium concentration ([Na ϩ ]) [F ϭ 38.9; P Ͻ 0.0001], which verified both pharmacological activation and inhibition of the V2R at the kidney collecting duct. Plasma osmolality and [Na ϩ ] demonstrated significant exercise (F ϭ 26.0 and F ϭ 11.1; P Ͻ 0.0001) and condition (F ϭ 5.1 and F ϭ 3.8; P Ͻ 0.05) effects (osmolality and [Na ϩ ], respectively). No significant exercise or condition effects were noted for either sweat or salivary [Na ϩ ]. Significant exercise effects were noted for plasma [AVP] (F ϭ 22.3; P Ͻ 0.0001), peak core temperature (F ϭ 103.3; P Ͻ 0.0001), percent body weight change (F ϭ 6.3; P ϭ 0.02), plasma volume change (F ϭ 21.8; P Ͻ 0.0001), and thirst rating (F ϭ 78.2; P Ͻ 0.0001). Performance time was not altered between conditions (P ϭ 0.80). In summary, AVP acting at V2R does not appear to regulate water losses from body fluids other than renal excretion during exercise. arginine vasopressin; sweat sodium; V2 antagonist; running ARGININE VASOPRESSIN (AVP) is the primary neuroendocrine regulator of water metabolism, acting to maintain plasma osmolality within the normal physiological range of 275-295 mosmol/kg H 2 O (38). Osmotic regulation of plasma tonicity generally occurs through activation of the vasopressin type 2 receptor (V2R) in the kidney. Activation of V2R initiates the translocation and subsequent insertion of aquaporin-2 (AQP2) water channels into the apical membrane of the collecting duct principal cells. This allows for water reabsorption along osmotic gradients and concomitant antidiuresis when plasma tonicities are high (46).Unlike this well-characterized interaction of V2R-stimulated translocation of AQP2 channels in the kidney, a regulatory effect of ...

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confidence: 99%

Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise

Hew‐Butler

Hummel

Rider

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It could be argued that the kidneys are trying to conserve water due to the additional loss in sweat during hot weather, but a study is needed to establish whether the kidneys excrete the same amount of solutes in such conditions. The analogy with the nephron is strengthened by the demonstration by Fasciolo et al that antidiuretic hormone (ADH) can inhibit sweating when introduced sub-dermally [18].…”

Section: The Sweat Gland Functioning As Nephronmentioning

confidence: 99%

Can sweat glands act as temporary or permanent replacement for the excretory function of kidney?

2017

ELSR

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Uremic frost -the powdery whitish substance, comprising urea and uric acid salts, on the skin of some patients with end stage kidney disease could be an attempt by the sweat glands to take over the function of the failing kidneys. Currently end stage kidney disease is managed mainly by hemodialysis and eventually kidney transplantation. Kidneys are primarily the organs for excretion of metabolic wastes. A normal kidney contains 800,000 to 1.5 million nephrons. This excretory function, which is essential for life, consists of filtration and selective reabsorption / secretion to produce urine. The major nitrogenous waste in urine is urea. The sweat glands are basically organs of thermoregulation. However, they are also involved in excretion of metabolic wastes. The total number of sweat glands lies between 1.6 and 4.5 million. There are anatomical and physiological similarities between the nephron -the functional unit of the kidney and the sweat gland. This article proposes a functional similarity between the two. Anatomically, the sweat gland bears some resemblance to the nephron. A nephron has 2 basic components, the glomerulus and the tubules. Similarly, the sweat gland has a secretory unit consisting of a base rolled into a glomerulus, and a duct that carries the sweat away. Both the kidneys and the sweat glands excrete nitrogenous wastes, water and electrolytes. They are also involved in maintaining acid-base balance. The hypothesis is that the skin, via the sweat glands, constitutes an alternative excretory organ to the kidneys, though probably minor, and thus could act as temporary or permanent replacement for the kidneys.

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“…O hormônio antidiurético, através de injeções intradér-micas, provoca vasoconstrição e aumento da permeabilidade das células do ducto glandular 10 . Há movimento de água do meio hipotônico dentro da glândula para o meio isotônico do líquido intersticial.…”

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“…Há movimento de água do meio hipotônico dentro da glândula para o meio isotônico do líquido intersticial. Como conseqüência, o volume de suor se reduz e sua concentração de sódio aumenta 10,12 .…”

Section: Comentáriosunclassified

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Abnormal sweat test in patient with Diabetes Insipidus unresponsive to ADH

Ma²,

Miasaki³

et al. 1995

J Pediatr (Rio J)

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Increased sweat concentrations (92, 76 e 80 mEq/l) were observed in a 7-year-old boy with pitressin-resistant diabetes insipidus. All previous observations of elevated sweat electrolytes in diabetes insipidus have been in infants less than 10 months of age. The sweat test is an exceptionally reliable, sensitive and specific test for the diagnosis of Cystic Fibrosis. Pitressin-resistant diabetes insipidus is one of the diseases associated with elevated sweat test results.

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Antidiuretic hormone and human eccrine sweating.

Cited by 32 publications

References 0 publications

Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise

Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise

Can sweat glands act as temporary or permanent replacement for the excretory function of kidney?

Abnormal sweat test in patient with Diabetes Insipidus unresponsive to ADH

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