ALPHA(1)-ADRENOCEPTOR AND ALPHA(2)-ADRENOCEPTOR ACTIONS OF PHENTOLAMINE AND PRAZOSIN ON BREATHING MOVEMENTS IN FETAL SHEEP IN-UTERO

Citation
Da. Giussani et al., ALPHA(1)-ADRENOCEPTOR AND ALPHA(2)-ADRENOCEPTOR ACTIONS OF PHENTOLAMINE AND PRAZOSIN ON BREATHING MOVEMENTS IN FETAL SHEEP IN-UTERO, Journal of physiology, 486(1), 1995, pp. 249-255
Citations number
21
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
486
Issue
1
Year of publication
1995
Pages
249 - 255
Database
ISI
SICI code
0022-3751(1995)486:1<249:AAAAOP>2.0.ZU;2-5
Abstract
1. We studied the effects of systemic administration of the alpha(1)- and alpha(2)-adrenoreceptor antagonist phentolamine and the selective alpha(1)-adrenoreceptor antagonist prazosin on fetal breathing movemen ts (PBM) and electrocortical activity (ECoG) in fetal sheep. In one gr oup of fetuses (group I; n = 7) the effects of phentolamine were measu red during normoxia and hypoxia. In the second group of fetuses (group II; n = 8) the effects of either phentolamine, or combined phentolami ne and prazosin, or prazosin alone, were measured during normoxia. 2. In group I fetuses, the incidence of FBM increased after phentolamine treatment. An increase in the incidence and mean episode duration of l ow-voltage ECoG (LV-ECoG) was also measured after phentolamine treatme nt. These effects of phentolamine persisted during hypoxia. 3. In grou p II fetuses a pronounced decrease in the incidence of FBM occurred af ter administration of prazosin following either phentolamine or saline pretreatment. These effects of prazosin on BBM were independent of an effect on ECoG activity. 4. We conclude that catecholamines have a st imulatory role on PBM mediated via an alpha(1)-adrenoreceptor mechanis m. Phentolamine leads to an increase in PBM by preferentially antagoni zing presynaptic alpha(2)-adrenoreceptors over postsynaptic alpha(1)-a drenoreceptors. This influence of phentolamine on FBM may be secondary to its effect on ECoG. Promotion of LV-ECoG by catecholamines is medi ated via an alpha(1)-independent mechanism.