Role of the alpha2-adrenoceptors on the pulmonary circulation in the ovine fetus
| Autor: | Yvon Riou, Véronique Houfflin-Debarge, Philippe Deruelle, Laurent Storme, Serge Klosowski, Sophie Jaillard, Eric Magnenant |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
medicine.medical_specialty
Pulmonary Circulation Vasodilation Gestational Age Nitroarginine Nitric oxide Norepinephrine (medication) chemistry.chemical_compound Norepinephrine Pregnancy Receptors Adrenergic alpha-2 medicine.artery Internal medicine Quinoxalines medicine Animals Enzyme Inhibitors Adrenergic alpha-Antagonists Fetus Sheep biology business.industry Yohimbine Nitric oxide synthase Endocrinology medicine.anatomical_structure chemistry Brimonidine Tartrate Pediatrics Perinatology and Child Health Pulmonary artery biology.protein Vascular resistance Female Nitric Oxide Synthase business Adrenergic alpha-Agonists medicine.drug |
| Zdroj: | Pediatric research. 54(1) |
| ISSN: | 0031-3998 |
| Popis: | Recent in vitro studies reported that nitric oxide release and pulmonary vasorelaxation can be mediated by endothelial alpha2-adrenoceptor activation. As norepinephrine (alpha1-,alpha2-, and beta1-adrenoceptor agonist) was found to induce pulmonary vasodilation in the ovine fetus, we hypothesized that alpha2-adrenoceptors may modulate basal pulmonary vascular tone and mediate the vascular effect of norepinephrine during fetal life. To determine the role of alpha2-adrenoceptors and the mechanisms of norepinephrine-mediated vasodilation in the fetal pulmonary circulation, we tested, in chronically prepared late-gestation fetal lambs, the hemodynamic response to 1). yohimbine (alpha2 antagonist); 2). UK 14304 (alpha2 agonist) with and without l-nitro-arginine (nitric oxide synthase inhibitor); and 3). norepinephrine infusion with and without yohimbine. We found that yohimbine increased mean pulmonary artery pressure by 15% (p < 0.05), decreased pulmonary flow by 22% (p < 0.01), and increased pulmonary vascular resistance by 51% (p < 0.01). UK 14304 increased pulmonary flow by 145% (p < 0.01) and decreased pulmonary vascular resistance by 58% (p < 0.01). l-Nitro-arginine abolished the UK 14304-mediated pulmonary vasodilation. Norepinephrine (0.5 microg x kg(-1)x min(-1) increased both pulmonary flow by 61% (p < 0.01) and pulmonary arterial pressure by 13% (p < 0.01) and decreased pulmonary vascular resistance by 33% (p < 0.01). Yohimbine abolished the norepinephrine-induced pulmonary vasodilation. This study suggests that 1). a basal alpha2-adrenoceptor activation-induced pulmonary vasodilation exists during fetal life; 2). the pulmonary vascular effects of alpha2-adrenoceptor activation are related at least in part to nitric oxide production; and 3). the norepinephrine-mediated pulmonary vasodilation involves alpha2-adrenoceptor activation. As a surge of norepinephrine exists at birth, we speculate that norepinephrine and endothelial alpha2-adrenoceptor activation may play a significant role in pulmonary vasodilation at birth. |
| Databáze: | OpenAIRE |
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