Journal Article•
Hypertension and pregnancy.
About: This article is published in Transactions of the Medical Society of London.The article was published on 1965-01-01 and is currently open access. It has received 47 citations till now. The article focuses on the topics: Pregnancy.
Citations
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TL;DR: A first step would be to subdivide preeclampsia into early‐onset disease (< 34 + 0 weeks') and late onset disease (> 34 +0 weeks').
Abstract: Preeclampsia is a heterogeneous disorder, and as with other diseases (e.g., type I and type II diabetes), progress in the understanding of this disorder would be assisted greatly if subtypes could be characterized. We suggest that a first step would be to subdivide preeclampsia into early‐onset disease ( 34 + 0 weeks').
700 citations
Cites background from "Hypertension and pregnancy."
...The intervillous space of the mismatched placenta releases factor(s) into the maternal circulation (intervillous soup (7)), leading to endothelial dysfunction and microangiopathic hemolysis (12), inflammatory mediator release (13), and neutrophil activation (14–17)....
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...It is likely that the maternal syndrome of preeclampsia is a final common pathway with many alternative routes to its inception (6,7)....
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...The resultant uteroplacental mismatch (7), where the demands of the pregnancy outstrip the capacity of the maternal arterial supply, may also arise due to excessive fetal demands, as occurs in multiple pregnancy (9) or fetal overgrowth (10), or by the loss of functioning placental mass in the setting of thrombophilia (11)....
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TL;DR: In this paper, a non-invasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha was used to determine prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension.
Abstract: Patients who develop pregnancy-induced hypertension exhibit a lesser increment in prostacyclin biosynthesis than healthy pregnant subjects. Whether this precedes the development of clinical disease and therefore may be important in the pathogenesis of pregnancy-induced hypertension or is a secondary event is unknown. We prospectively determined prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension by use of noninvasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha. Patients were recruited at less than 20 weeks gestation. After delivery, patients were retrospectively allocated by use of preset criteria, to one of four groups: pregnancy-induced hypertension (n = 12), hypertension in labor (n = 22), chronic hypertension (n = 9), and normotension (n = 24). There was a significant increase in prostacyclin biosynthesis in all study groups during gestation. However, patients who developed pregnancy-induced hypertension exhibited a lesser increment and this difference persisted throughout gestation. These results are consistent with a pathophysiologic role for altered prostacyclin biosynthesis in women with pregnancy-induced hypertension. In addition, decreased prostacyclin formation identifies a population at risk of developing pregnancy-induced hypertension. Such information would assist the design of clinical trials of drugs, such as aspirin, that might prevent the development of this disease.
263 citations
TL;DR: The discovery of the aquaporin-1 (AQP1) water channel by Agre and colleagues led to the Nobel Prize in 2003 and the identification of other water channels in the kidney, namely AQP2, 3.
Abstract: The discovery of the aquaporin-1 (AQP1) water channel by Agre and colleagues ([1][1],[2][2]), which led to the Nobel Prize in 2003, has revolutionized the understanding of body fluid water regulation by the kidney. Moreover, the identification of other water channels in the kidney, namely AQP2, 3,
177 citations
Cites background from "Hypertension and pregnancy."
...cellular fluid ranging from 30 to 50% (46)....
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TL;DR: It is demonstrated that estrogens increase the affinity of α-adrenergic receptors in blood vessels, and evidence that the estrogen-induced increase in vascular sensitivity to catecholamine-induced contraction is mediated, at least in part, by these affinity changes is provided.
Abstract: Wilson S. Colucci, Michael A. Gimbrone, Jr., Margaret K. McLaughlin, William Halpern, and R. Wayne Alexander From the Cardiovascular Divison and the Vascular Pathophysiology Laboratory, Brigham and Women's Hospital, the Departments of Medicine and Pathology, Harvard Medical School, Boston, Massachusetts; and Departments of Obstetrics and Gynecology and of Physiology and Biophysics, University of Vermont Medical Center, Burlington, Vermont
162 citations
TL;DR: Pregnancy in patients with cirrhosis faces unique risks, including higher rates of spontaneous abortion and prematurity and a potential for life‐threatening variceal hemorrhage, hepatic decompensation, splenic artery aneurysm rupture, and postpartum hemorrhage.
160 citations
References
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TL;DR: A first step would be to subdivide preeclampsia into early‐onset disease (< 34 + 0 weeks') and late onset disease (> 34 +0 weeks').
Abstract: Preeclampsia is a heterogeneous disorder, and as with other diseases (e.g., type I and type II diabetes), progress in the understanding of this disorder would be assisted greatly if subtypes could be characterized. We suggest that a first step would be to subdivide preeclampsia into early‐onset disease ( 34 + 0 weeks').
700 citations
TL;DR: In this paper, a non-invasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha was used to determine prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension.
Abstract: Patients who develop pregnancy-induced hypertension exhibit a lesser increment in prostacyclin biosynthesis than healthy pregnant subjects. Whether this precedes the development of clinical disease and therefore may be important in the pathogenesis of pregnancy-induced hypertension or is a secondary event is unknown. We prospectively determined prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension by use of noninvasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha. Patients were recruited at less than 20 weeks gestation. After delivery, patients were retrospectively allocated by use of preset criteria, to one of four groups: pregnancy-induced hypertension (n = 12), hypertension in labor (n = 22), chronic hypertension (n = 9), and normotension (n = 24). There was a significant increase in prostacyclin biosynthesis in all study groups during gestation. However, patients who developed pregnancy-induced hypertension exhibited a lesser increment and this difference persisted throughout gestation. These results are consistent with a pathophysiologic role for altered prostacyclin biosynthesis in women with pregnancy-induced hypertension. In addition, decreased prostacyclin formation identifies a population at risk of developing pregnancy-induced hypertension. Such information would assist the design of clinical trials of drugs, such as aspirin, that might prevent the development of this disease.
263 citations
TL;DR: The discovery of the aquaporin-1 (AQP1) water channel by Agre and colleagues led to the Nobel Prize in 2003 and the identification of other water channels in the kidney, namely AQP2, 3.
Abstract: The discovery of the aquaporin-1 (AQP1) water channel by Agre and colleagues ([1][1],[2][2]), which led to the Nobel Prize in 2003, has revolutionized the understanding of body fluid water regulation by the kidney. Moreover, the identification of other water channels in the kidney, namely AQP2, 3,
177 citations
TL;DR: It is demonstrated that estrogens increase the affinity of α-adrenergic receptors in blood vessels, and evidence that the estrogen-induced increase in vascular sensitivity to catecholamine-induced contraction is mediated, at least in part, by these affinity changes is provided.
Abstract: Wilson S. Colucci, Michael A. Gimbrone, Jr., Margaret K. McLaughlin, William Halpern, and R. Wayne Alexander From the Cardiovascular Divison and the Vascular Pathophysiology Laboratory, Brigham and Women's Hospital, the Departments of Medicine and Pathology, Harvard Medical School, Boston, Massachusetts; and Departments of Obstetrics and Gynecology and of Physiology and Biophysics, University of Vermont Medical Center, Burlington, Vermont
162 citations
TL;DR: Pregnancy in patients with cirrhosis faces unique risks, including higher rates of spontaneous abortion and prematurity and a potential for life‐threatening variceal hemorrhage, hepatic decompensation, splenic artery aneurysm rupture, and postpartum hemorrhage.
160 citations