Decreased heat tolerance is associated with hypothalamo-pituitary-adrenocortical axis impairment

Neuroscience. 2007 Jun 29;147(2):522-31. doi: 10.1016/j.neuroscience.2007.04.035. Epub 2007 May 24.

Abstract

When rats are exposed to heat, they adapt themselves to the stressor with a wide inter-individual variability. Such differences in heat tolerance may be related to particularities in the hypothalamo-pituitary-adrenocortical (HPA) axis activation. To further this hypothesis, 80 rats instrumented with a telemetric device for abdominal temperature (Tabd) measurement were separated into two groups. Sixty-eight rats were exposed during 90 min at an ambient temperature of 40 degrees C, and 12 rats to an ambient temperature of 22 degrees C. Heat-exposed rats were then divided into three groups using the a posteriori k-means clustering method according to their Tabd level at the end of heat exposure. Heat tolerant rats (Tol, n=30) exhibiting the lowest Tabd showed a slight dehydration, a moderate triglyceride mobilization, but the highest plasma adrenocorticotropic-hormone (ACTH) and corticosterone levels. Conversely, heat exhausted rats (HE, n=14) presented the highest Tabd, a higher degree of dehydration, a greater metabolic imbalance with the lowest plasma triglyceride level and the highest lactate concentration, as well as a lowest plasma corticosterone and ACTH levels. The fact that the proopiomelanocortin (POMC) mRNA content within the pituitary was low despite of a high c-fos mRNA level is also relevant. Current inflammatory processes in HE rats were underlined by lower inhibitory factor kappaBalpha (IkappaBalpha) mRNA and higher tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA. In conclusion, data show that intolerance to heat exposure is associated to an HPA axis impairment, possibly related to changes occurring in the IkappaBalpha and TNF-alpha mRNA levels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenocorticotropic Hormone / blood
  • Animals
  • Calcium Signaling / physiology
  • Corticosterone / blood
  • Corticotropin-Releasing Hormone / biosynthesis
  • Corticotropin-Releasing Hormone / genetics
  • Gene Expression / physiology
  • Genes, Immediate-Early / genetics
  • HSP70 Heat-Shock Proteins / biosynthesis
  • HSP70 Heat-Shock Proteins / genetics
  • Heat Stress Disorders / physiopathology*
  • Hematocrit
  • Hypothalamo-Hypophyseal System / physiopathology*
  • Inflammation Mediators / metabolism
  • Intracellular Signaling Peptides and Proteins
  • Male
  • Pituitary-Adrenal System / physiopathology*
  • Pro-Opiomelanocortin / biosynthesis
  • Pro-Opiomelanocortin / genetics
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Telemetry
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics

Substances

  • HSP70 Heat-Shock Proteins
  • Inflammation Mediators
  • Intracellular Signaling Peptides and Proteins
  • RCAN1 protein, rat
  • RNA, Messenger
  • Transcription Factors
  • Pro-Opiomelanocortin
  • Adrenocorticotropic Hormone
  • Corticotropin-Releasing Hormone
  • Corticosterone