Data/hora: 02/06/2024 10:32:25

Provedor de dados: | 56
País: | Brazil
Título: | Neuronal and endothelial nitric oxide synthase gene knockout mice
Autores: | Huang,P.L.
Data: | 1999-11-01
Ano: | 1999
Palavras-chave: | Nitric oxide; Targeted disruption; Gene knockout; Endothelium; Stroke; Atherosclerosis.
Resumo: | Targeted disruption of the neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) genes has led to knockout mice that lack these isoforms. These animal models have been useful to study the roles of nitric oxide (NO) in physiologic processes. nNOS knockout mice have enlarged stomachs and defects in the inhibitory junction potential involved in gastrointestinal motility. eNOS knockout mice are hypertensive and lack endothelium-derived relaxing factor activity. When these animals are subjected to models of focal ischemia, the nNOS mutant mice develop smaller infarcts, consistent with a role for nNOS in neurotoxicity following cerebral ischemia. In contrast, eNOS mutant mice develop larger infarcts, and show a more pronounced hemodynamic effect of vascular occlusion. The knockout mice also show that nNOS and eNOS isoforms differentially modulate the release of neurotransmitters in various regions of the brain. eNOS knockout mice respond to vessel injury with greater neointimal proliferation, confirming that reduced NO levels seen in endothelial dysfunction change the vessel response to injury. Furthermore, eNOS mutant mice still show a protective effect of female gender, indicating that the mechanism of this protection cannot be limited to upregulation of eNOS expression. The eNOS mutant mice also prove that eNOS modulates the cardiac contractile response to ß-adrenergic agonists and baseline diastolic relaxation. Atrial natriuretic peptide, upregulated in the hearts of eNOS mutant mice, normalizes cGMP levels and restores normal diastolic relaxation.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999001100005
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X1999001100005
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.32 n.11 1999
Fonte: | info:eu-repo/semantics/openAccess