| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print August 15, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00328.2002
Submitted on June 5, 2002
Accepted on August 9, 2002
1 Department of Physiology, Faculty of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, SP, Brazil
2 Department of Morphology, Estomatology and Physiology, Dental School of Ribeirao Preto - University of Sao Paulo, Ribeirao Preto, SP, Brazil
* To whom correspondence should be addressed. E-mail: branco{at}forp.usp.br.
Hypoxia evokes a regulated decrease in body temperature, a response that has been termed anapyrexia, but the mechanisms involved are poorly understood. Therefore, the present study was undertaken to test the hypothesis that hypoxia-induced anapyrexia results from the activation of cyclic AMP (cAMP)- and cyclic GMP (cGMP)-dependent pathways in the preoptic region (PO). Adult male Wistar rats weighing 230-260 g were used. Body temperature was monitored by biotelemetry and the levels of cAMP and cGMP were determined in the anteroventral third ventricular region (AV3V), where the PO is located. Using immunohistochemistry, we observed that the PO contains a high density of cAMP- and cGMP-containing cells. Interestingly, hypoxia exposure raised the levels of cAMP and cGMP in the AV3V. Intra-PO microinjection of Rp-cAMPS, an inhibitor of cAMP-dependent protein kinase, attenuated hypoxia-induced anapyrexia. Similarly, intra-PO microinjection of the mixed B-adrenoceptor/5-HT1A receptor antagonist, propranolol, also impaired the drop in body temperature in response to hypoxia. The reduction in body temperature evoked by intra-PO serotonin, but not epinephrine, was blocked by Rp-cAMPS, indicating the involvement of a preoptic serotonin-cAMP pathway in the development of anapyrexia. Moreover, microinjection of L-monomethyl-L-arginine, an inhibitor of nitric oxide (NO) synthesis, or Rp-cGMPS, an inhibitor of cGMP-dependent protein kinase, into the PO also attenuated hypoxia-induced anapyrexia. In conclusion, the present study supports that hypoxia-induced anapyrexia results from the activation of the serotonin-cAMP and NO-cGMP pathways in the PO.
This article has been cited by other articles:
|
|
 |
|
  C. L. Wright, P. W. Burgoon, G. A. Bishop, and J. A. Boulant Cyclic GMP alters the firing rate and thermosensitivity of hypothalamic neurons Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1704 - R1715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Chevrier, L. Bourdon, and F. Canini Cosignaling of adenosine and adenosine triphosphate in hypobaric hypoxia-induced hypothermia Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2006; 290(3): R595 - R600. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. J. Kaiyala and D. S. Ramsay Assessment of heat production, heat loss, and core temperature during nitrous oxide exposure: a new paradigm for studying drug effects and opponent responses Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2005; 288(3): R692 - R701. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
