Preservation of serotonin-mediated contractility in adult sheep pulmonary arteries following long-term high-altitude hypoxia.

Long-term hypoxia (LTH) can increase serotonin (5-HT) signaling as well as extracellular calcium entry in adult rodent pulmonary arteries (PA), and 5-HT is associated with pulmonary hypertension. Because LTH, 5-HT, and calcium entry are related, we tested the hypothesis that LTH increases 5-HT-mediated PA contractility and associated calcium influx through L-type Ca2+ channels, nonselective cation channels (NSCC), and reverse-mode sodium-Ca2+ exchange. We performed wire myography and confocal calcium imaging on pulmonary arteries from adult ewes that lived near sea level or were maintained at high-altitude (3801 m) for ∼110 days.

Long-term maternal hypoxia: the role of extracellular Ca2+ entry during serotonin-mediated contractility in fetal ovine pulmonary arteries.

Antenatal maternal long-term hypoxia (LTH) can alter serotonin (5-HT) and calcium (Ca(2+)) signaling in fetal pulmonary arteries (PAs) and is associated with persistent pulmonary hypertension of the newborn (PPHN). In humans, the antenatal maternal hypoxia can be secondary to smoking, anemia, and chronic obstructive pulmonary disorders. However, the mechanisms of antenatal maternal hypoxia-related PPHN are unresolved.

Risk Factors of Early and Late Onset Preeclampsia among Thai Women.

BACKGROUND: Little research has been conducted to specifically identify risk factors of early and late onset preeclampsia among Thai women. OBJECTIVE: To examine risk factors of early and late onset of preeclampsia among Thai women. METHODS: A case-control study of 150 preeclampsia cases with an equal number of normotensive controls was conducted among women who delivered live born singleton infants at King Chulalongkorn Memorial Hospital, Rajavithi Hospital, and Police General Hospital in Bangkok, Thailand from July 2006 to November 2007.

Placental insufficiency results in temporal alterations in the renin angiotensin system in male hypertensive growth restricted offspring.

Reduced uterine perfusion initiated in late gestation in the rat results in intrauterine growth restriction (IUGR) and development of hypertension by 4 wk of age. We hypothesize that the renin angiotensin system (RAS), a regulatory system important in the long-term control of blood pressure, may be programmed by placental insufficiency and may contribute to the etiology of IUGR hypertension. We previously reported that RAS blockade abolished hypertension in adult IUGR offspring; however, the mechanisms responsible for the early phase of hypertension are unresolved.