Mechanism of cold diuresis in the rat

Morgan, Monica L; Ellis, M. A.; Berl, Tomás

doi:10.1152/ajprenal.1983.244.2.f210

Cited by 17 publications

(10 citation statements)

References 8 publications

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“…The diuresis was not due to a diminished response to AVP. The glomerular filtration rate, renal blood flow, Na+ excretion, and osmolar clearance were equivalent during control and cold conditions [119]. In anesthetized rats hypothermia (Tre 28°C) increased the urine flow (sixfold) and urine Na+ excretion (sevenfold) and decreased urine osmolality and plasma AVP level (-50%).…”

Section: Insulin Glucagon Glucosementioning

confidence: 87%

“…Nonosmotic suppression of AVP in response to cold exposure has been noted in animals [97,119,120] and humans [59,121], and may be the basis of the cold diuresis. Cold exposure (4°C) for 30min increased systolic blood pressure and plasma NE (twofold) level and decreased the plasma volume (-7.8% ) and plasma AVP level (-35 % ) in men with no change in Tre• The changes in systolic blood pressure, NE, and AVP were significant as early as 2min after the beginning of exposure.…”

Section: Insulin Glucagon Glucosementioning

confidence: 99%

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Endocrine Responses to Heat and Cold Stress

Matsumoto

Nishiyama

Nishimura

et al. 2001

Thermotherapy for Neoplasia, Inflammation, and Pain

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Summary. This review focuses on the endocrine responses to thermal stimuli during passive heat or cold exposure, with particular reference to the relation of these responses to the changes in the body core temperature (Teare). Mild to moderate hyperthermia (<1°C rise in Teare) induces the release of growth hormone and prolactin (PRL). Moderate hypothermia (la_2°C fall in Teore) suppresses PRL release. A positive correlation between plasma PRL and Teare suggests some role for PRL in thermoregulation. Hypothermia activates the hypothalamo-pituitary-thyroid (HPT) axis and releases thyrotropin-releasing hormone, thyroid-stimulating hormone (TSH), and thyroid hormones and increases the metabolic rate. Enhancement of extrathyroidal production of triiodothyronine (T3) from thyroxine (T4) may precede the TSH response to cold. Both severe hyperthermia and hypothermia (1°_3°C changes in Teare) activate the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in release of corticotropin-releasing factor, adrenocorticotropic hormone, cortisol, and norepinephrine. The responses in the HPT axis and the HPA axis are not apparent in humans, as they are in rats, probably owing to the larger body mass of humans. Hyperthermia stimulates the renin-angiotensin-aldosterone system and the release of arginine vasopressin (AVP) and atrial natriuretic peptide, but this might be due to nonthermal factors. Diuresis due to suppression of AVP release is induced by cold. Gonadal response to thermal stimuli is possibly suppressive. The hormonal responses induced by thermal stress are mostly dependent on the change in Teare in humans; in small animals they are also dependent on the change in skin temperature. I ntrod uctionBody core temperature (Teare) may increase during physical exercise and passive heating (while sauna bathing, with head-out water immersion, and exposure to hot environments); it decreases during cold exposure. Changes in Teare induce various endocrine responses to maintain homeostasis of the body. Recently, local and whole-body hyperthermia therapy for cancer and some benign diseases and induced hypothermia treatment to protect the important organs from hypoxic damage have been developed and widely utilized. On these occasions, the endocrine responses induced by the changes in Teare should be considered. Hormonal responses and their relation to the immune system during exercise in the heat and passive hyperthermia have been reviewed [1][2][3], but little attention has been paid to the relation of endocrine responses to the change in Teare. Body heating and cooling paradigms may include concurrent psychological stress. This review focuses on the endocrine responses to thermal stimuli during passive heating and cooling, with particular reference to their relation to changes in Teare. The study was undertaken to elucidate the thermal influence alone, excluding the influence of non thermal stress. Growth HormoneThere have been many consistent findings that hyperthermia induces a rapid rise in ci...

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Section: Insulin Glucagon Glucosementioning

confidence: 87%

Section: Insulin Glucagon Glucosementioning

confidence: 99%

Endocrine Responses to Heat and Cold Stress

Matsumoto

Nishiyama

Nishimura

et al. 2001

Thermotherapy for Neoplasia, Inflammation, and Pain

View full text Add to dashboard Cite

show abstract

“…This diuresis was seen 60 min after the animals were placed in the cold and would correspond well to our own electrophysiological and urine flow findings. More recently, Morgan et al (1983) reported a diuresis in cold-exposed rats over a 45 min time period. Thus, it would appear that, in most previous studies, only single urine samples were taken over more lengthy sampling periods which may, in part, explain the conflicting results.…”

Section: Discussionmentioning

confidence: 97%

“…Decreased levels of this hormone have been reported in humans (Segar & Moore, 1968) and rats (Morgan, Anderson, Ellis & Berl, 1983), whereas increased levels in unanaesthetized dogs (Sadowski et al 1972) and no consistent changes in young pigs (Forsling et al 1976) have been observed.…”

Section: Introductionmentioning

confidence: 97%

Effect of cooling on supraoptic neurohypophysial neuronal activity and on urine flow in the rat.

Ferguson¹,

Pittman²,

Riphagen³

1984

The Journal of Physiology

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SUMMARY1. The activity of antidromically identified supraoptic neurosecretory neurones was recorded in Sprague-Dawley rats under urethane or sodium pentobarbitone anaesthesia during cooling of the body with a cold pack.2. Of twelve phasic neurones studied during a complete cooling and rewarming cycle, six displayed an initial increase, followed by a depression in activity during the period of reduced body temperature. The remaining six phasic neurones did not alter their activity during cooling.3. Non-phasic neurohypophysial neurones displayed a reversible reduction (n = 8), or increase (n = 6) in activity during cooling, while seven neurones were unaffected by changes in body temperature.4. In four other anaesthetized Sprague-Dawley rats, urine flow was reduced by approximately 50 % during cooling; this was followed by a diuresis after removal of the cold pack and return of body temperature to normal. The antidiuresis did not occur in homozygous Brattleboro rats which lack arginine vasopressin. 5. The electrophysiological data from a proportion of the supraoptic neurohypophysial neurones correlate with the observed changes in urine flow.

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“…Acute and chronic exposures to cold induced diuresis probably via different mechanisms: the former via a reduction in plasma AVP (2,10,13) and the latter by suppression of renal V 2 receptors without reduction of plasma AVP. Kidney weights of LE and VD rats were increased equally by cold exposure, suggesting that AVP may not be involved in coldinduced renal hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension

Sun

2006

American Journal of Physiology-Renal Physiology

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Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25 degrees C, warm). After the control period, one LE group and one VD group were exposed to cold (5 degrees C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.

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Mechanism of cold diuresis in the rat

Cited by 17 publications

References 8 publications

Endocrine Responses to Heat and Cold Stress

Endocrine Responses to Heat and Cold Stress

Effect of cooling on supraoptic neurohypophysial neuronal activity and on urine flow in the rat.

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension

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