Nitric oxide as a peripheral and central mediator in temperature regulation

Simón, E.

doi:10.1007/bf01345248

Cited by 37 publications

(18 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, a reduction in core temperature greatly augments sympathetic activity with further vasoconstriction during sustained cold exposure and cold acclimatization (70). Nitric oxide has been shown to be a mediator of temperature regulation (93) and is depressed in expired gas during cold stress (78).…”

Section: Cold Watermentioning

confidence: 99%

“…Acclimatization increases maximal tissue insulation by peripheral vasoconstriction and may be either centrally or locally controlled (56). Nitric oxide has been suggested to play an important role in the thermally induced vasoconstriction (93). An additional response to reduced skin and core temperatures is the initiation of shivering, generating more metabolic heat (56).…”

Section: Cold Watermentioning

confidence: 99%

See 1 more Smart Citation

The underwater environment: cardiopulmonary, thermal, and energetic demands

Pendergast¹,

Lundgren²

2009

Journal of Applied Physiology

134

View full text Add to dashboard Cite

Pendergast DR, Lundgren CE. The underwater environment: cardiopulmonary, thermal, and energetic demands. J Appl Physiol 106: 276 -283, 2009. First published November 26, 2008 doi:10.1152/japplphysiol.90984.2008.-Water covers over 75% of the earth, has a wide variety of depths and temperatures, and holds a great deal of the earth's resources. The challenges of the underwater environment are underappreciated and more short term compared with those of space travel. Immersion in water alters the cardio-endocrine-renal axis as there is an immediate translocation of blood to the heart and a slower autotransfusion of fluid from the cells to the vascular compartment. Both of these changes result in an increase in stroke volume and cardiac output. The stretch of the atrium and transient increase in blood pressure cause both endocrine and autonomic changes, which in the short term return plasma volume to control levels and decrease total peripheral resistance and thus regulate blood pressure. The reduced sympathetic nerve activity has effects on arteriolar resistance, resulting in hyperperfusion of some tissues, which for specific tissues is time dependent. The increased central blood volume results in increased pulmonary artery pressure and a decline in vital capacity. The effect of increased hydrostatic pressure due to the depth of submersion does not affect stroke volume; however, a bradycardia results in decreased cardiac output, which is further reduced during breath holding. Hydrostatic compression, however, leads to elastic loading of the chest wall and negative pressure breathing. The depthdependent increased work of breathing leads to augmented respiratory muscle blood flow. The blood flow is increased to all lung zones with some improvement in the ventilation-perfusion relationship. The cardiac-renal responses are time dependent; however, the increased stroke volume and cardiac output are, during head-out immersion, sustained for at least hours. Changes in water temperature do not affect resting cardiac output; however, maximal cardiac output is reduced, as is peripheral blood flow, which results in reduced maximal exercise performance. In the cold, maximal cardiac output is reduced and skin and muscle are vasoconstricted, resulting in a further reduction in exercise capacity. respiratory; renal; immersion; exercise; aging; sex differences; submersion; pressure; energy cost THE UNDERWATER ENVIRONMENT is unique, and while it is a magical place with great history and beauty and plant and animal life and holds a wealth of resources, it also imposes pronounced physiological stresses on humans and animals. This brief review offers an overview of how the major environmental challenges, i.e., the pressure, temperature extremes, and the unbreathable ambient medium, of the "Silent World" affect circulation, renal system and water balance, breathing, exercise, and thermal balance and how it imposes some threats due to pharmacological or toxic effects of respired gases at high pressure, i.e., great depths. Adaptations to ...

show abstract

Section: Cold Watermentioning

confidence: 99%

Section: Cold Watermentioning

confidence: 99%

The underwater environment: cardiopulmonary, thermal, and energetic demands

Pendergast¹,

Lundgren²

2009

Journal of Applied Physiology

134

View full text Add to dashboard Cite

show abstract

“…19,65,70,73,74). Previous data regarding its potential role in fever have, however, been conflicting, some indicating no effect (31,57) and others pyretic (3, 5, 40 -43, 53) or antipyretic (20,46,50,56,60,76) effects.…”

Section: Discussionmentioning

confidence: 99%

“…10 and 49) have prompted suggestions that NO could have a propyretic function in the central mediation of the febrile response to pyrogens (for reviews, see Refs. 19,65,70,73,and 74). Indeed, the three isoforms of nitric oxide synthase [endothelial (e), neural (n), and inducible (i) NOS], the enzyme that converts L-arginine to citrulline and NO, occur in the hypothalamus (7,22), and circulating bacterial endotoxic lipopolysaccharides (LPS) and pyrogenic cytokines stimulate the release of NO in the preoptic (POA, the fever-producing locus) and paraventricular regions of the hypothalamus (23,37,64,67,80,85,88).…”

mentioning

confidence: 99%

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Feleder¹,

Perlik²,

Blatteis³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and NO induces cyclooxygenase (COX)-2-dependent PGE2, we investigated whether NO mediates the production of this central fever mediator. Conscious guinea pigs with intra-POA microdialysis probes received LPS intravenously (2 μg/kg) and, thereafter, an NO donor (SIN-1) or scavenger (carboxy-PTIO) intra-POA (20 μg/μl each, 2 μl/min, 6 h). Core temperature (Tc) was monitored constantly; dialysate NE and PGE2 were analyzed in 30-min collections. To verify the reported involvement of α2-adrenoceptors (AR) in PGE2 production, clonidine (α2-AR agonist, 2 μg/μl) was microdialyzed with and without SIN-1 or carboxy-PTIO. To assess the possible involvement of oxidative NE and/or NO products in the demonstrated initially COX-2-independent POA PGE2 increase, (+)-catechin (an antioxidant, 3 μg/μl) was microdialyzed, and POA PGE2, and Tc were determined. SIN-1 and carboxy-PTIO reduced and enhanced, respectively, the rises in NE, PGE2, and Tc produced by intravenous LPS. Similarly, they prevented and increased, respectively, the delayed elevations of PGE2 and Tc induced by intra-POA clonidine. (+)-Catechin prevented the LPS-induced elevation of PGE2, but not of Tc. We conclude that the antipyretic activity of NO derives from its inhibitory modulation of the LPS-induced release of POA NE. These data also implicate free radicals in POA PGE2 production and raise questions about its role as a central LPS fever mediator.

show abstract

“…It is one of biological messengers that can serve peripherally as well as in the central nervous system [15]. In addition, there is accumulating evidence for NO being involved in temperature regulation in homeotherms.…”

Section: Introductionmentioning

confidence: 99%

Leptin immunoexpression and innervation in rat interscapular brown adipose tissue of cold-acclimated rats: the effects of L-arginine and L-NAME.

Korać

Buzadžić²,

Petrović³

et al. 2008

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Abstract:The aim of the present study was to explore the effect of nitric oxide on leptin immunoexpression and innervation in interscapular brown adipose tissue (IBAT) of room-and cold-acclimated rats. Animals acclimated both to roomtemperature (22 ± 1°C) and cold (4 ± 1°C) were treated with L-arginine, a substrate for nitric oxide synthases (NOSs), or N?-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOSs, for 45 days. Leptin expression and localization in brown adipocytes was studied by immunohistochemistry, and innervation stained by the Bodian method. Strong leptin immunopositivity was observed in brown adipocytes cytoplasm of all room-acclimated groups, but nuclear leptin positivity was found only in L-NAME treated rats. In cold-acclimated control and L-NAME treated rats leptin immunopositivity was absent, while L-arginine treatment reversed the cold-induced suppression of leptin expression. Comparing to control, L-arginine, and even more L-NAME, at 22 ± 1°C induced greater innervation. In conclusion, L-arginine treatment changes leptin expression pattern on cold in rat IBAT.

show abstract

Nitric oxide as a peripheral and central mediator in temperature regulation

Cited by 37 publications

References 24 publications

The underwater environment: cardiopulmonary, thermal, and energetic demands

The underwater environment: cardiopulmonary, thermal, and energetic demands

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Leptin immunoexpression and innervation in rat interscapular brown adipose tissue of cold-acclimated rats: the effects of L-arginine and L-NAME.

Contact Info

Product

Resources

About