Sarah L Hissen1,2, Qi Fu3,4. 1. Women's Heart Health Laboratory, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Avenue, Suite 435, Dallas, TX, 75231, USA. 2. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA. 3. Women's Heart Health Laboratory, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Avenue, Suite 435, Dallas, TX, 75231, USA. QiFu@TexasHealth.org. 4. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA. QiFu@TexasHealth.org.
Abstract
PURPOSE: Previous microneurographic studies found that muscle sympathetic nerve activity (MSNA) increased in normotensive pregnant women and was even greater in women with gestational hypertension and preeclampsia during the third trimester. It is possible that sympathetic activation during the latter months of normal pregnancy helps return arterial pressure to non-pregnant levels. However, when the increase in sympathetic activity is excessive, hypertension ensues. The key question that must be addressed is whether sympathetic activation develops early during pregnancy and remains high throughout gestation, or whether this sympathetic overactivity only occurs at term, providing the substrate for preeclampsia and other pregnancy-associated cardiovascular complications. METHODS: This was a literature review of autonomic neural control during pregnancy. RESULTS: Recent work from our laboratory and other laboratories showed that in healthy women resting MSNA increased in early pregnancy, increased further in late pregnancy, and returned to the pre-pregnancy levels shortly after delivery. We found that women who exhibited excessive sympathetic activation during the first trimester, before any clinical signs and symptoms appeared, developed gestational hypertension at term. We also found that the level of corin, an atrial natriuretic peptide-converting enzyme, was increased in the maternal circulation, especially during late pregnancy, as a homeostatic response to elevated sympathetic activity. CONCLUSION: These findings provide important insight into the neural mechanisms underlying hypertensive disorders during pregnancy. With this knowledge, early prevention or treatment targeted to the appropriate pathophysiology may be initiated, which may reduce maternal and fetal death or morbidity, as well as cardiovascular risks in women later in life.
PURPOSE: Previous microneurographic studies found that muscle sympathetic nerve activity (MSNA) increased in normotensive pregnant women and was even greater in women with gestational hypertension and preeclampsia during the third trimester. It is possible that sympathetic activation during the latter months of normal pregnancy helps return arterial pressure to non-pregnant levels. However, when the increase in sympathetic activity is excessive, hypertension ensues. The key question that must be addressed is whether sympathetic activation develops early during pregnancy and remains high throughout gestation, or whether this sympathetic overactivity only occurs at term, providing the substrate for preeclampsia and other pregnancy-associated cardiovascular complications. METHODS: This was a literature review of autonomic neural control during pregnancy. RESULTS: Recent work from our laboratory and other laboratories showed that in healthy women resting MSNA increased in early pregnancy, increased further in late pregnancy, and returned to the pre-pregnancy levels shortly after delivery. We found that women who exhibited excessive sympathetic activation during the first trimester, before any clinical signs and symptoms appeared, developed gestational hypertension at term. We also found that the level of corin, an atrial natriuretic peptide-converting enzyme, was increased in the maternal circulation, especially during late pregnancy, as a homeostatic response to elevated sympathetic activity. CONCLUSION: These findings provide important insight into the neural mechanisms underlying hypertensive disorders during pregnancy. With this knowledge, early prevention or treatment targeted to the appropriate pathophysiology may be initiated, which may reduce maternal and fetal death or morbidity, as well as cardiovascular risks in women later in life.