Plasma vasopressin, oxytocin, estradiol, and progesterone related to water and sodium excretion in normal pregnancy and gestational hypertension

Risberg, Anitha; Olsson, Kerstin; Lyrenäs, Sven; Sjöquist, Mats

doi:10.1080/00016340902919002

Cited by 31 publications

(29 citation statements)

References 27 publications

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“…Although 3 groups of investigators found no deficiency of progesterone in association with PE 23,24 ), a group from Sweden provided evidence that plasma progesterone increased until week 24 in normotensive and hypertensive women with further increase in normotensive women as compared with the hypertensive group. 25 Our group found evidence of progesterone deficiency in patients with severe forms of PE and supplementation of sera with progesterone blunted PE-induced endothelial cell activation from vascular endothelial cells. Importantly, administration of 17-OHPC to placental ischemic rats decreased mean arterial pressure without decreasing pup weight or litter size.…”

Section: Commentmentioning

confidence: 82%

Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia

Kiprono

Wallace

Moseley

et al. 2013

American Journal of Obstetrics and Gynecology

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OBJECTIVE Preeclampsia (PE) is associated with hypertension and elevated endothelin (ET-1), an indicator of endothelial cell activation and dysfunction. Reduction of uteroplacental perfusion (RUPP) in the pregnant rat model of PE is characterized by elevated mean arterial pressure, inflammatory cytokines, and activation of the ET-1 system. We aim to determine whether 17-alpha-hydroxyprogesterone caproate (17-OHPC) or progesterone suppresses these pathways. STUDY DESIGN Plasma progesterone was purified from normal pregnant (NP) and PE patients and measured via enzyme-linked immunosorbent assay. Human umbilical vein endothelial cells were exposed to the sera with or without progesterone added and ET-1 was measured. Pregnant rats underwent the RUPP procedure with or without intraperitoneal 17-OHPC. Mean arterial pressure was compared in RUPP vs NP rats. Human umbilical vein endothelial cells were exposed to NP or RUPP sera, with and without progesterone and ET-1 measured. RESULTS Progesterone was significantly decreased in PE women compared with NP women. In response to human sera, ET-1 was elevated in PE women compared to NP women, and decreased with addition of progesterone. Mean arterial pressure was significantly elevated in RUPP vs NP rats but was attenuated by 17-OHPC. ET-1 secretion was stimulated significantly by RUPP compared to NP rat sera, but attenuated by progesterone. CONCLUSION Circulating progesterone is significantly lower in PE women compared to controls. 17-OHPC attenuates hypertension in response to placental ischemia in RUPP rats. Progesterone blunts vascular ET-1 stimulated at cellular level by sera from PE women or RUPP rats. Decreased circulating progesterone is associated with stimulation of ET-1. 17-OHPC supplementation blunts hypertension and progesterone blunts endothelial cell ET-1 secretion in response to placental ischemia.

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Section: Commentmentioning

confidence: 82%

Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia

Kiprono

Wallace

Moseley

et al. 2013

American Journal of Obstetrics and Gynecology

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“…This is an important finding, as the peripartum-associated changes in EPCs and the microvasculature of the PVN might play an important role in enhanced availability of the neurohypophyseal hormones AVP and OXT during the peripartum period by increasing their cytoplasmatic transport from the luminal to the abdominal side of the membrane. Indeed, OXT plasma concentrations have been shown to be diminished in women with gestational hypertension [78]. As hormones like AVP and OXT have been shown to be implicated in mechanisms of cell volume regulation in rodents [79], it might be that PVN OXT neurons modulate their own capillary blood supply and vice versa .…”

Section: Structural Functional and Molecular Plasticity Of The Bmentioning

confidence: 99%

The Maternal Brain: An Organ with Peripartal Plasticity

et al. 2014

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The time of pregnancy, birth, and lactation, is characterized by numerous specific alterations in several systems of the maternal body. Peripartum-associated changes in physiology and behavior, as well as their underlying molecular mechanisms, have been the focus of research since decades, but are still far from being entirely understood. Also, there is growing evidence that pregnancy and lactation are associated with a variety of alterations in neural plasticity, including adult neurogenesis, functional and structural synaptic plasticity, and dendritic remodeling in different brain regions. All of the mentioned changes are not only believed to be a prerequisite for the proper fetal and neonatal development, but moreover to be crucial for the physiological and mental health of the mother. The underlying mechanisms apparently need to be under tight control, since in cases of dysregulation, a certain percentage of women develop disorders like preeclampsia or postpartum mood and anxiety disorders during the course of pregnancy and lactation. This review describes common peripartum adaptations in physiology and behavior. Moreover, it concentrates on different forms of peripartum-associated plasticity including changes in neurogenesis and their possible underlying molecular mechanisms. Finally, consequences of malfunction in those systems are discussed.

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“…An orchestrated network of vasodilator substances, including nitric oxide (NO), prostacyclin (PGI 2 ), EDHF, kallikrein, angiotensin-(1-7), and VEGF, may participate in the local and systemic hemodynamic adaptations during pregnancy (82,86). Estrogen (E 2 ) levels also increase during pregnancy (23,74). E 2 induces long-term genomic vascular effects, such as stimulation of endothelial cell growth, upregulation of endothelial NO synthase and NO production, increased cyclooxygenase (COX) activity and PGI 2 production (19,53,64,77), inhibition of vascular smooth muscle (VSM) proliferation, and downregulation of VSM Ca 2ϩ channels and PKC (33,61).…”

Section: The Present Study Describes Pregnancy-associated Increases Imentioning

confidence: 99%

Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy

Mata

Reslan

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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RA. Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy. Am J Physiol Heart Circ Physiol 309: H1679 -H1696, 2015. First published September 25, 2015 doi:10.1152/ajpheart.00532.2015.-Normal pregnancy is associated with adaptive hemodynamic, hormonal, and vascular changes, and estrogen (E 2) may promote vasodilation during pregnancy; however, the specific E 2 receptor (ER) subtype, post-ER signaling mechanism, and vascular bed involved are unclear. We tested whether pregnancy-associated vascular adaptations involve changes in the expression/ distribution/activity of distinct ER subtypes in a blood vessel-specific manner. Blood pressure (BP) and plasma E 2 were measured in virgin and pregnant (day 19) rats, and the thoracic aorta, carotid artery, mesenteric artery, and renal artery were isolated for measurements of ER␣, ER␤, and G protein-coupled receptor 30 [G protein-coupled ER (GPER)] expression and tissue distribution in parallel with relaxation responses to E 2 (all ERs) and the specific ER agonist 4,4=,4Љ-(4-propyl-[1H]-pyrazole-1,3,5-triyl)-tris-phenol (PPT; ER␣), diarylpropionitrile (DPN; ER␤), and G1 (GPER). BP was slightly lower and plasma E 2 was higher in pregnant versus virgin rats. Western blots revealed increased ER␣ and ER␤ in the aorta and mesenteric artery and GPER in the aorta of pregnant versus virgin rats. Immunohistochemistry revealed that the increases in ERs were mainly in the intima and media. In phenylephrineprecontracted vessels, E 2 and PPT caused relaxation that was greater in the aorta and mesenteric artery but similar in the carotid and renal artery of pregnant versus virgin rats. DPN-and G1-induced relaxation was greater in the mesenteric and renal artery than in the aorta and carotid artery, and aortic relaxation to G1 was greater in pregnant versus virgin rats. The nitric oxide synthase inhibitor N -nitro-L-arginine methyl ester with or without the cyclooxygenase inhibitor indomethacin with or without the EDHF blocker tetraethylammonium or endothelium removal reduced E 2, PPT, and G1-induced relaxation in the aorta of pregnant rats, suggesting an endothelium-dependent mechanism, but did not affect E 2-, PPT-, DPN-, or G1-induced relaxation in other vessels, suggesting endothelium-independent mechanisms. E 2, PPT, DPN, and G1 caused relaxation of Ca 2ϩ entry-dependent KCl contraction, and the effect of PPT was greater in the mesenteric artery of pregnant versus virgin rats. Thus, during pregnancy, an increase in ER␣ expression in endothelial and vascular smooth muscle layers of the aorta and mesenteric artery is associated with increased ER␣-mediated relaxation via endothelium-derived vasodilators and inhibition of Ca 2ϩ entry into vascular smooth muscle, supporting a role of aortic and mesenteric arterial ER␣ in pregnancyassociated vasodilation. GPER may contribute to aortic relaxation while enhanced ER␤ expression could mediate other genomic vascular effects during pregnancy.

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Plasma vasopressin, oxytocin, estradiol, and progesterone related to water and sodium excretion in normal pregnancy and gestational hypertension

Abstract: The low plasma vasopressin and increasing plasma oxytocin concentrations with unchanged water and sodium excretion indicate that oxytocin assists vasopressin in concentrating urine during pregnancy.

Cited by 31 publications

References 27 publications

Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia

Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia

The Maternal Brain: An Organ with Peripartal Plasticity

Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy

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