|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Depto. de Bioquimica y Biologia Molecular y Fisiologia, Universidad de Valladolid, Valladolid, Spain; Instituto de Biologia y Genetica Molecular, Consejo Superior de Investigaciones Cientificas (CSIC), Valladolid, Spain
* To whom correspondence should be addressed. E-mail: rrigual{at}ibgm.uva.es.
Hypoxia elicits catecholamine (CA) secretion from the adrenal medulla (AM) in perinatal animals by acting directly on chromaffin cells. However, it is debated if the innervation of the AM, which in the rat occurs in the second postnatal week, suppresses this direct hypoxic response; opioid peptides have been proposed as mediators of this suppression. To resolve these controversies, we have compared CA secretory responses to high [K+]e and hypoxia in AMs of neonatal (1-2 days) and juvenile (14-15 and 30 days) rats superfused in vitro. Additionally, it was studied the effect of hypercapnia/ acidosis on the CA secretory responses in the AM during postnatal development and the possible interaction between acidic and hypoxic stimuli. Responses to high [K+]e were comparable at all ages, but those to hypoxia and hypercapnia/acidosis were maximal in neonatal animals. Suppression of hypoxic response in the rat AM is not mediated by opioids since their agonists did not affect the hypoxic CA response. Association of acidosis and hypoxia, mimicking the episodes of asphyxia occurring during delivery, generates a more than additive secretory response in neonatal AM. Our data confirm the loss of the direct sensitivity to hypoxia of the AM in the initial weeks of life and demonstrate a direct response of neonatal AM to hypercapnia/acidosis. The synergistic effect between hypoxia and acidosis would explain the CA outburst seen in naturally delivered mammals crucial for adaptation to extrauterine life.
This article has been cited by other articles:
![]() |
J. Buttigieg, S. Brown, M. Zhang, M. Lowe, A. C. Holloway, and C. A. Nurse Chronic nicotine in utero selectively suppresses hypoxic sensitivity in neonatal rat adrenal chromaffin cells FASEB J, May 1, 2008; 22(5): 1317 - 1326. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Buttigieg, S. T. Brown, M. Lowe, M. Zhang, and C. A. Nurse Functional mitochondria are required for O2 but not CO2 sensing in immortalized adrenomedullary chromaffin cells Am J Physiol Cell Physiol, April 1, 2008; 294(4): C945 - C956. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. K. Kumar, V. Rai, S. D. Sharma, D. P. Ramakrishnan, Y.-J. Peng, D. Souvannakitti, and N. R. Prabhakar Chronic intermittent hypoxia induces hypoxia-evoked catecholamine efflux in adult rat adrenal medulla via oxidative stress J. Physiol., August 15, 2006; 575(1): 229 - 239. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |