Cold-Induced Salt Intake in Mice and Catecholamine, Renin and Thermogenesis Mechanisms

Dejima, Yasushi; Fukuda, Satoru; Ichijoh, Yuuka; Takasaka, Kouichi; Ohtsuka, Ryoichi

doi:10.1006/appe.1996.0016

Cited by 16 publications

(14 citation statements)

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“…This finding is intriguing given that stress (6)(7)(8)(9) and systemic administration of ACTH (24) have been shown to cause clear-cut increases in Na intake. In contrast to these results in sheep, ICV, but not systemic, infusion of ovine CRF increased Na intake of rabbits (20) and mice (9).…”

Section: Discussionmentioning

confidence: 82%

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The inhibitory effect of hormones associated with stress on Na appetite of sheep

Weisinger

Blair‐West

Burns

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Stress is a large stimulus of Na appetite in rabbits, rats, and mice. This study investigated the influence of some peptides implicated in stress, i.e., adrenocorticotropin (ACTH), corticotropin-releasing factor (CRF), and the recently discovered member of the CRF family, urocortin, on the ingestive behavior of sheep. Intracerebroventricular infusion of these peptides over 4 days decreased the need-free Na intake of Na-repleted sheep. Intracerebroventricular infusion of urocortin, however, did not alter Na intake of Na-depleted sheep. Systemic infusion of ACTH increased, whereas systemic infusion of either urocortin or CRF decreased, Na intake of Na-repleted sheep. The increase in Na intake caused by the peripheral infusion of ACTH was blocked by concurrent i.v. infusion of urocortin, substantiating the inhibitory role of this peptide on Na appetite. Central administration of all peptides and i.v. administration of urocortin or urocortin and ACTH combined decreased food intake. Water intake was not directly influenced by the peptides. Rather, decreased water intake, when observed, was secondary to decreased food intake, as determined by pair-feeding experiments. Whereas systemic infusion of ACTH mimics the increase in Na intake observed in several different stressful situations, CRF and urocortin actually inhibit Na intake, indicating a direct central action overriding any effect of these peptides on ACTH release. Indeed, the inhibition of Na intake by urocortin occurred despite its stimulation of ACTH release and the subsequent increase in peripheral level of cortisol. Thus it would appear that hormones associated with stress have both excitatory and inhibitory influences on Na intake. Presumably, other physiological processes entrained by stress also will be important in determining the quantitative outcome on Na appetite.

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Section: Discussionmentioning

confidence: 82%

“…Stress can cause an increase in Na intake (6)(7)(8)(9) and, in some instances, a decrease in food intake (10,11). Corticotropin-releasing factor (CRF), a 41-aa peptide originally isolated from the ovine hypothalamus (12), is one factor involved in the initiation of the various behavioral and physiological responses to stress (1,2,4,5).…”

mentioning

confidence: 99%

The inhibitory effect of hormones associated with stress on Na appetite of sheep

Weisinger

Blair‐West

Burns

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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“…Furthermore, extrahypothalamic CRH increases dopamine neurotransmission in the nucleus accumbens and may contribute to the reinforcing effects of cocaine (19). Central injections of CRH and experimental stressors increase salt intake in several species as well (7,8,28,50,53,54). However, VP is also released both centrally and peripherally as part of the stress response and could therefore contribute equally to these behaviors if they are the result of a stressor (10,11).…”

Section: Discussionmentioning

confidence: 94%

Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl

McBride¹,

Flynn²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Prior sodium restriction cross-sensitizes rats to the psychomotor effects of amphetamines and vice versa. Repeated central injections of vasopressin (VP) induce a psychomotor sensitization similar to amphetamine sensitization and repeated sodium deficiency. Thus brain VP signaling may be a common mechanism involved in mediating these two motivational systems. In experiment 1, we tested the hypothesis that rats previously sensitized to central VP would show enhanced psychomotor responses to amphetamine. Rats were administered saline, VP (50 ng), or amphetamine (1 mg/kg or 3 mg/kg) on days 1 and 2, and given saline or amphetamine on day 3. Amphetamine produced psychomotor arousal in all groups. However, amphetamine on day 3 elicited a significantly greater psychomotor response in rats that had prior injections of amphetamine or VP than in rats previously treated with saline. In experiment 2, the hypothesis that prior experience with central VP would cross-sensitize rats to drinking hypertonic sodium (NaCl) solutions was tested. Rats were administered VP (50 ng) or saline for 3 days. On the fourth day, nondeprived rats were given access to 0.3 M NaCl and water for 1 h. Control and saline-treated rats only drank 1 ml of 0.3 M NaCl, but rats previously exposed to central VP drank significantly more hypertonic saline (4 ml). These results show that prior experience with central VP cross-sensitizes rats to the psychomotor stimulant effects of amphetamine and the ingestion of concentrated NaCl solutions. This pattern of cross-sensitization links central VP signaling, amphetamine, and sodium deficiency, and therefore it may play a role in the cross-sensitization between sodium appetite and amphetamines.

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“…Sympathetic input to the kidney increases the release of renin, which in tum contributes to the production of AGII. PRA and NE concentrations in the kidney increased after a 6-h cold exposure (8°C) in mice [124]. Plasma AGII concentration increased 10-fold 4h after cold exposure (4°C), returned to control levels at days 1 and 3 of cold exposure, and was again increased (twofold) at 7 days of cold exposure in rats.…”

Section: Insulin Glucagon Glucosementioning

confidence: 88%

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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Cold-Induced Salt Intake in Mice and Catecholamine, Renin and Thermogenesis Mechanisms

Cited by 16 publications

References 0 publications

The inhibitory effect of hormones associated with stress on Na appetite of sheep

The inhibitory effect of hormones associated with stress on Na appetite of sheep

Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl

Endocrine Responses to Heat and Cold Stress

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