Pathophysiology of hypertension during preeclampsia linking placental ischemia with endothelial dysfunction.
Hypertension
; 38(3 Pt 2): 718-22, 2001 Sep.
Article
en En
| MEDLINE
| ID: mdl-11566964
Studies over the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal-pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during preeclampsia are still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiological mechanisms responsible for the elevation in arterial pressure in women with preeclampsia.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Placenta
/
Preeclampsia
/
Endotelio Vascular
/
Hipertensión
Tipo de estudio:
Etiology_studies
/
Prognostic_studies
Límite:
Female
/
Humans
/
Pregnancy
Idioma:
En
Revista:
Hypertension
Año:
2001
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos