Fasudil inhibits the myogenic response in the fetal pulmonary circulation
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چکیده
منابع مشابه
Fasudil inhibits the myogenic response in the fetal pulmonary circulation.
In addition to high pulmonary vascular resistance (PVR) and low pulmonary blood flow, the fetal pulmonary circulation is characterized by mechanisms that oppose vasodilation. Past work suggests that high myogenic tone contributes to high PVR and may contribute to autoregulation of blood flow in the fetal lung. Rho-kinase (ROCK) can mediate the myogenic response in the adult systemic circulation...
متن کاملInhibition of 20-HETE abolishes the myogenic response during NOS antagonism in the ovine fetal pulmonary circulation.
Mechanisms that maintain high pulmonary vascular resistance (PVR) and oppose vasodilation in the fetal lung are poorly understood. In fetal lambs, increased pulmonary artery pressure evokes a potent vasoconstriction, suggesting that a myogenic response contributes to high PVR in the fetus. In adult systemic circulations, the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) ...
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Primary essential hypertension is second only to diabetic nephropathy as a etiology for end-stage renal disease.1 In addition, coexistent/superimposed hypertension plays a major role in the progression of most forms of chronic kidney disease (CKD), including diabetic nephropathy.2–5 Nevertheless, the individual risk is very low, with 1% of the hypertensive population developing end-stage renal ...
متن کاملFetal and neonatal pulmonary circulation.
During fetal life, gas exchange is carried out in the placenta. The lung does not have a physiological role, apart from possible metabolic functions which include secretion of hormones, enzymatic conversion of inactive substances to functional hormones, and degradation of active materials to inactive metabolites. Blood flow through the lungs is quite low during fetal life; most of the systemic ...
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ژورنال
عنوان ژورنال: American Journal of Physiology-Heart and Circulatory Physiology
سال: 2008
ISSN: 0363-6135,1522-1539
DOI: 10.1152/ajpheart.00490.2008