pituitrin and Pre-Eclampsia

Pregnancy and early life create specific psychosomatic challenges for the mother and child, such as changes in hemodynamics, resetting of the water-electrolyte balance, hypoxia, pain, and stress, that all play an important role in the regulation of the release of oxytocin and vasopressin. Both of these hormones regulate the water-electrolyte balance and cardiovascular functions, maturation of the cardiovascular system, and cardiovascular responses to stress. These aspects may be of particular importance in a state of emergency, such as hypertension in the mother or severe heart failure in the child. In this review, we draw attention to a broad spectrum of actions exerted by oxytocin and vasopressin in the pregnant mother and the offspring during early life. To this end, we discuss the following topics:

Topics: Animals; Female; Heart Failure; Humans; Infant, Newborn; Oxytocin; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Vasopressins; Water-Electrolyte Balance

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.

Topics: Blood Volume; Cardiac Output; Cardiac Output, Low; Edema; Female; Fibrosis; Humans; Kidney; Natriuresis; Nephrotic Syndrome; Pre-Eclampsia; Pregnancy; Renin-Angiotensin System; Sympathetic Nervous System; Vascular Resistance; Vasodilation; Vasopressins

Topics: Adrenocorticotropic Hormone; Aldosterone; Blood Volume; Edema; Extracellular Space; Female; Glomerulonephritis; Humans; Hyaluronoglucosaminidase; Kidney; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenal Cortex Hormones; Animals; Biopsy; Body Weight; Diet, Sodium-Restricted; Eclampsia; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Nephritis; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pyelonephritis; Sodium; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Glands; Aldosterone; Diagnosis, Differential; Edema; Extracellular Space; Female; Heart Diseases; Humans; Kidney; Kidney Diseases; Liver Cirrhosis; Male; Parasitic Diseases; Pituitary Gland; Posture; Pre-Eclampsia; Pregnancy; Pulmonary Edema; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aldosterone; Angiotensin II; Blood Coagulation Disorders; Catecholamines; Diagnosis, Differential; Estrogens; Female; Humans; Kidney Diseases; Placenta; Placenta Diseases; Pre-Eclampsia; Pregnancy; Renin; Serotonin; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Female; Humans; Hypertension, Renal; Kidney; Kidney Diseases; Norepinephrine; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Renin; Time Factors; Vasopressins

To investigate associations between plasma oxytocin and vasopressin concentrations and renal water and sodium excretion during normal pregnancy in comparison with gestational hypertension.. A prospective open trial conducted in the 12th, 24th, and 36th weeks of gestation.. Seven antenatal clinics in Sweden.. Thirty-seven normotensive women, 15 women with gestational hypertension, and five women with mild preeclampsia.. Hormones were analyzed with radioimmunoassay. Albumin, osmolality, sodium, and urea were analyzed by routine methods.. Blood pressure was elevated in the hypertensive women and body mass index in mild preeclampsia from week 12. Renal sodium excretion did not differ between groups or weeks and mean renal free water clearance was negative. In normotensive women, the vasopressin concentration was 1.1+/-0.2 (week 12) and 0.7+/-0.1 pmol/L (week 36: p = 0.053). In hypertensive women, vasopressin concentration was 1.7+/-1.0 pmol/L, week 12, and 0.7+/-0.1 pmol/L in week 36 (ns). In normotensive women, oxytocin concentration increased from 23+/-1 pmol/L in week 12 to 48+/-3 pmol/L in week 36 (p<0.001). Corresponding values in hypertensive women were 36+/-11 (week 12) and 55+/-5 pmol/L (week 36: ns). In all groups, plasma estradiol concentration increased. Plasma progesterone increased until week 24 in normotensive and hypertensive women with further increase in normotensive women.. 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.

Topics: Estradiol; Female; Humans; Hypertension, Pregnancy-Induced; Kidney; Oxytocin; Pre-Eclampsia; Pregnancy; Progesterone; Vasopressins; Water-Electrolyte Balance

An enzyme-linked immunosorbent assay is described for the measurement of ouabain in human plasma. This assay is specific for ouabain, strophanthidin, and ouabagenin, with other steroids, including digoxin and vasopressor hormones, exhibiting negligible cross-reactivity. Assay sensitivity was 0.06 nmol/L if 1 mL plasma was extracted and less than 0.005 nmol/L when 20 mL plasma was analyzed. Extracted plasma samples showed ouabainlike immunoreactivity that diluted in parallel with the ouabain standard curve. Repeated extraction and assay of single plasma samples, however, did not produce consistent results in the assay. Increased specificity was obtained by high-performance liquid chromatography of sample extracts before assay. When high-performance liquid chromatographic profiles of plasma spiked with ouabain standard or following bolus intravenous injections of ouabain into normal human volunteers were compared with profiles of unspiked plasma, there was no support for the immunoreactive material in the latter samples being ouabain. We propose that if ouabain is present in the human circulation, its concentration is less than 0.005 nmol/L.

Topics: Animals; Antibodies; Antibody Specificity; Chromatography, High Pressure Liquid; Cross Reactions; Digoxin; Enzyme-Linked Immunosorbent Assay; Female; Fetal Blood; Heart Failure; Humans; Kidney Failure, Chronic; Ouabain; Pre-Eclampsia; Pregnancy; Rabbits; Sensitivity and Specificity; Steroids; Strophanthidin; Vasopressins

Preeclampsia (PE) is a disease of pregnancy characterized by early onset of maternal hypertension and proteinuria. New findings indicate that arginine vasopressin (AVP) may be a contributing factor to ignite PE. The aim of this study was to identify if there is any correlation between arginine vasopressin promoter polymorphisms and PE.. Venous blood samples of 100 PE and 100 normal pregnant women were obtained for DNA extraction to identify the polymorphisms of AVP promoter by RFLP and nested-PCR techniques.. rs3729965 polymorphism of PE women was detected to have significant correlation with body mass index (BMI) (P = 0.028).. Statistical analysis of three polymorphisms namely rs3729965, rs61138008 and rs3761249 of preeclamptic women (PEW) and none preeclamptic pregnant women (NPEW) revealed that rs3729965 genotypic distribution was significantly different between both groups (P = 0.04). Further analysis revealed that rs3729965 CT genotype of PEW had significant correlation to their BMI (P = 0.028).. Polymorphic variants located on the promoter region of AVP are associated with PE. Thus we hypothesize that allelic variation may have a role in increasing the risk of developing PE.

Topics: Adolescent; Adult; Female; Genetic Predisposition to Disease; Humans; Iran; Neurophysins; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; Polymorphism, Single Nucleotide; Pre-Eclampsia; Pregnancy; Promoter Regions, Genetic; Protein Precursors; Vasopressins; White People; Young Adult

Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.. We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.. Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.

Topics: Animals; Blood Pressure; Female; Ischemia; Placenta; Postpartum Period; Pre-Eclampsia; Pregnancy; Rats; Sodium Chloride, Dietary; Vasopressins

Copeptin, a marker of arginine vasopressin (AVP) secretion, is elevated throughout human pregnancies complicated by preeclampsia (PE), and AVP infusion throughout gestation is sufficient to induce the major phenotypes of PE in mice. Thus, we hypothesized a role for AVP in the pathogenesis of PE. AVP infusion into pregnant C57BL/6J mice resulted in hypertension, renal glomerular endotheliosis, intrauterine growth restriction, decreased placental growth factor (PGF), altered placental morphology, placental oxidative stress, and placental gene expression consistent with human PE. Interestingly, these changes occurred despite a lack of placental hypoxia or elevations in placental fms-like tyrosine kinase-1 (FLT1). Coinfusion of AVP receptor antagonists and time-restricted infusion of AVP uncovered a mid-gestational role for the AVPR1A receptor in the observed renal pathologies, versus mid- and late-gestational roles for the AVPR2 receptor in the blood pressure and fetal phenotypes. These findings demonstrate that AVP is sufficient to initiate phenotypes of PE in the absence of placental hypoxia, and indicate that AVP may mechanistically (independently, and possibly synergistically with hypoxia) contribute to the development of clinical signs of PE in specific subtypes of human PE. Additionally, they identify divergent and gestational time-specific signaling mechanisms that mediate the development of PE phenotypes in response to AVP.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Blood Pressure; Blood Pressure Determination; Cell Hypoxia; Disease Models, Animal; Female; Humans; Mice; Mice, Inbred C57BL; Neurophysins; Placenta; Plethysmography; Pre-Eclampsia; Pregnancy; Protein Precursors; Receptors, Vasopressin; Recombinant Proteins; Vasopressins

The occurrence of electrolyte disorders as hypocalcemia and/or hyponatremia is an uncommon event in preeclampsia, which can be the sign of serious situation, with potentially unfavourable consequences for the mother and her fœtus. Hyponatremia in the setting of preeclampsia is an indicator of severity, and requires the understanding of the etiologic mechanisms to initiate an appropriate treatment. Indeed the often-considered fluid restriction is rarely a treatment option for pregnant women. Hypocalcemia is a complication that must be monitored when a treatment with high doses of intravenous magnesium sulphate is introduced. In this context, hypocalcemia must be sought, with the exclusion of other etiologies as vitamin D deficiency, hypoparathyroidism or renal and extrarenal loss of calcium. A replacement therapy, intravenous or oral according to circumstances, should be considered in case of severe or symptomatic hypocalcemia.

Topics: Adult; Aldosterone; Antihypertensive Agents; Capillary Leak Syndrome; Cesarean Section; Emergencies; Female; Fertilization in Vitro; Fetal Growth Retardation; Humans; Hypocalcemia; Hyponatremia; Infant, Newborn; Infusions, Intravenous; Labetalol; Magnesium Sulfate; Male; Pre-Eclampsia; Pregnancy; Pressoreceptors; Renin-Angiotensin System; Vasopressins

Preeclampsia, a cardiovascular disorder of late pregnancy, is characterized as a low-renin hypertensive state relative to normotensive pregnancy. Because other nonpregnant low-renin hypertensive disorders often exhibit and are occasionally dependent on elevated arginine vasopressin (AVP) secretion, we hypothesized a possible use for plasma AVP measurements in the prediction of preeclampsia. Copeptin is an inert prosegment of AVP that is secreted in a 1:1 molar ratio and exhibits a substantially longer biological half-life compared with AVP, rendering it a clinically useful biomarker of AVP secretion. Copeptin was measured throughout pregnancy in maternal plasma from preeclamptic and control women. Maternal plasma copeptin was significantly higher throughout preeclamptic pregnancies versus control pregnancies. While controlling for clinically significant confounders (age, body mass index, chronic essential hypertension, twin gestation, diabetes mellitus, and history of preeclampsia) using multivariate regression, the association of higher copeptin concentration and the development of preeclampsia remained significant. Receiver operating characteristic analyses reveal that as early as the sixth week of gestation, elevated maternal plasma copeptin concentration is a highly significant predictor of preeclampsia throughout pregnancy. Finally, chronic infusion of AVP during pregnancy (24 ng per hour) is sufficient to phenocopy preeclampsia in C57BL/6J mice, causing pregnancy-specific hypertension, renal glomerular endotheliosis, proteinuria, and intrauterine growth restriction. These data implicate AVP release as a novel predictive biomarker for preeclampsia very early in pregnancy, identify chronic AVP infusion as a novel and clinically relevant model of preeclampsia in mice, and are consistent with a potential causative role for AVP in preeclampsia in humans.

Topics: Adult; Animals; Arginine Vasopressin; Biomarkers; Blood Pressure; Disease Models, Animal; Early Diagnosis; Endothelium, Vascular; Female; Glycopeptides; Humans; Hypertension; Kidney Glomerulus; Male; Mice; Mice, Inbred C57BL; Pre-Eclampsia; Pregnancy; Proteinuria; ROC Curve; Time Factors; Vasopressins

This study was performed to establish whether microparticles from plasma of women with preeclampsia cause endothelial dysfunction, as described for isolated myometrial arteries in preeclampsia.. Myometrial arteries were isolated from biopsy specimens obtained at cesarean delivery from healthy pregnant women (n = 22) and mounted in a wire myograph. Bradykinin concentration-response curves were obtained before and after 1-hour incubation or after overnight incubation with one of the following preparations of plasma from individual women with preeclampsia (n = 16): Whole plasma, microparticle-free plasma, isolated microparticles resuspended in physiologic saline solution or physiologic saline solution. Overnight incubation was also performed with microparticles isolated from healthy pregnant women (n = 6). One-hour incubation was performed with 2% or 10% solution and overnight incubation with 5% solution.. No effect of preeclamptic plasma, with or without microparticles, on bradykinin-mediated relaxation was observed. Overnight, but not 1-hour, incubation with preeclamptic microparticles caused abolishment of bradykinin-mediated relaxation in contrast to healthy pregnant microparticles (P <.005).. Preeclamptic microparticles, but not healthy pregnant microparticles cause endothelial dysfunction in isolated myometrial arteries from healthy pregnant women after overnight incubation, whereas other preeclamptic plasma constituents protect the endothelium from this effect.

Topics: Adult; Arteries; Biopsy; Bradykinin; Cesarean Section; Endothelium, Vascular; Female; Gestational Age; Humans; Muscle Relaxation; Muscle, Smooth, Vascular; Myometrium; Pre-Eclampsia; Pregnancy; Reference Values; Vasoconstriction; Vasopressins

We aimed to compare placental small artery function from women with pre-eclampsia and normal pregnancy. In particular, we wished to test the hypothesis that these arteries respond differently to an endothelium-dependent vasodilator, to the presence of nitric oxide, and to the presence of cyclic monophosphate nucleotides.. A small vessel wire myograph was used to study placental arteries (200 to 550 microm). Contractile function was assessed with vasopressin. Relaxation was assessed with the endothelium-dependent vasodilator, bradykinin, and the endothelium-independent vasodilators sodium nitroprusside (a nitric oxide donor) and papaverine (a phosphodiesterase inhibitor).. The constrictor response to vasopressin did not differ between patient groups (p=0.79; repeated measures ANOVA). For both normal pregnancy and pre-eclampsia, the response of pre-constricted arteries to the endothelium-dependent vasodilator, bradykinin, was minimal. Vasorelaxation to sodium nitroprusside and papaverine was attenuated in pre-eclampsia compared to normal pregnancy (p=0.03 and p<0.001, respectively; repeated measures ANOVA).. In pre-eclampsia, placental arteries exhibit an attenuated vasodilatory response to nitric oxide.

Topics: Adult; Analysis of Variance; Arteries; Bradykinin; Chorion; Endothelium, Vascular; Female; Humans; Muscle Contraction; Muscle, Smooth, Vascular; Nitric Oxide; Nitroprusside; Papaverine; Placenta; Pre-Eclampsia; Pregnancy; Statistics, Nonparametric; Vascular Resistance; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

It has previously been observed that a circulating factor or factors may be responsible for the changes in vessel behavior that are postulated to underlie the pathogenesis of preeclampsia. We wished to ascertain whether such changes in endothelial function are dependent on the vascular bed under investigation.. Myometrial and infracolic omental vessels resistance vessels were obtained at cesarean delivery or hysterectomy. After incubation with either plasma from women with preeclampsia or plasma from normotensive pregnant women, myographic techniques were used to assess the endothelium-dependent relaxations of these vessels.. Incubation of myometrial vessels from normotensive pregnant women with plasma from women with preeclampsia resulted in a significant reduction in endothelium-dependent relaxation, an effect that was independent of the parity of the patients from whom the vessels had been taken. Incubation of omental vessels from normotensive pregnant women and myometrial vessels from nonpregnant women with plasma from women with preeclampsia had no effect on the endothelium-dependent relaxation observed.. This study demonstrates that the inducible changes in resistance vessel behavior are dependent on the tissue bed under investigation and on the pregnancy status of the patient.

Topics: Adult; Biopsy; Bradykinin; Cesarean Section; Endothelium, Vascular; Female; Gestational Age; Humans; Muscle Contraction; Muscle, Smooth, Vascular; Myography; Myometrium; Omentum; Pre-Eclampsia; Pregnancy; Statistics, Nonparametric; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

To compare the in vitro effect of plasma from normal pregnant women and women with pre-eclampsia on the endothelium-dependent behaviour of myometrial resistance arteries from normal pregnant women.. An in vitro comparative study.. Nottingham City Hospital.. Uterine biopsy specimens were obtained from normal pregnant women delivered by elective caesarean section at term. Plasma was collected from nulliparous women with pre-eclampsia (n = 18), and from multiparous normal pregnant women (n = 18), all samples being matched for maternal age and gestation at venepuncture. Pools of plasma from women with pre-eclampsia and normal pregnant women were formed from these samples and were used in all the experiments.. Myometrial resistance vessels obtained from the uterine biopsies were incubated with normal pregnant plasma, plasma from women with pre-eclampsia, or without plasma. Wire myography was employed to study the effect of plasma on the endothelium-dependent behaviour of these vessels.. Incubation of vessels from normal pregnant women with plasma from women with pre-eclampsia resulted in a significant reduction in endothelium-dependent relaxation, compared with vessels incubated either with plasma from normal pregnant women or without plasma. This alteration in endothelial function occurred after an incubation period of one hour and required a threshold concentration for its effect to become established. Removal of the vascular endothelium abolished these changes in vessel behaviour. There were no plasma-induced alterations in the endothelium-independent behaviour of the vascular smooth muscle.. This study supports the hypothesis that plasma from women with pre-eclampsia is capable of altering endothelium-dependent myometrial relaxation in vessels from pregnant women.

Topics: Adult; Bradykinin; Dose-Response Relationship, Drug; Endothelium, Vascular; Female; Humans; Myometrium; Plasma; Pre-Eclampsia; Pregnancy; Uterine Contraction; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

The study investigated whether an inducible alteration in endothelium-dependent relaxation in myometrial vessels could be correlated with plasma lipid composition.. Myometrial resistance vessels were obtained from 10 women with normal pregnancy undergoing elective cesarean delivery. Paired vessels were incubated with plasma samples from patients with preeclampsia or from women with normal pregnancy and mounted on a wire myograph. After contraction with vasopressin, the degree of relaxation in response to bradykinin was observed. Plasma samples were assayed for cholesterol, triglycerides, apolipoprotein A1, and apolipoprotein B.. A significant reduction in endothelium-dependent relaxation with respect to control values was observed in vessels incubated in plasma samples from patients with preeclampsia (P =.0001). Although no significant difference was noted between the lipid profiles of the 2 subgroups, a significant correlation was found between the vessel relaxation and the plasma content of apolipoprotein A1 (R2 = 0.36, P = .025).. Plasma samples from women with pregnancies complicated by preeclampsia are capable of altering endothelium-dependent myometrial vessel relaxation. A significant relationship between the apolipoprotein A1 concentration and endothelial behavior supports the suggestion that aberrant lipid metabolism may be involved in the endothelial dysfunction characteristic of preeclampsia.

Topics: Adult; Apolipoprotein A-I; Apolipoproteins B; Arteries; Bradykinin; Cholesterol; Female; Humans; Lipids; Muscle Contraction; Muscle, Smooth, Vascular; Myometrium; Pre-Eclampsia; Pregnancy; Triglycerides; Vascular Resistance; Vasopressins

To measure endothelium-dependent relaxation in myometrial resistance arteries and to compare this parameter in nonpregnant and normotensive pregnant women and those with pregnancies complicated by pre-eclampsia.. A prospective study.. Nottingham City Hospital.. Thirty-seven nonpregnant women undergoing hysterectomy and 51 pregnant women undergoing caesarean section, of whom there were 39 normotensive and 12 with pre-eclampsia.. Resistance arteries, dissected from myometrial biopsies, were mounted on a wire myograph and preconstricted with vasopressin then subjected to incremental doses of bradykinin.. Endothelium-dependent relaxation to bradykinin was seen in the vessels of nonpregnant and normotensive pregnant women. Markedly reduced endothelium-dependent relaxation was found in the myometrial arteries from women with pre-eclampsia when compared with both nonpregnant (P < 0.0001) and normotensive pregnant (P < 0.0001) women.. A significant loss of endothelium-dependent relaxation in myometrial resistance arteries in pre-eclampsia may contribute to the altered vasoreactivity seen in pre-eclampsia, and particularly to the decreased placental perfusion and fetal growth retardation commonly associated with this condition.

Topics: Adult; Arteries; Bradykinin; Dose-Response Relationship, Drug; Endothelium, Vascular; Female; Humans; Muscle Contraction; Muscle, Smooth, Vascular; Myography; Myometrium; Norepinephrine; Potassium; Pre-Eclampsia; Pregnancy; Prospective Studies; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

Both fetal and maternal blood pressure is regulated mainly by the humoral factor, vasoactive peptides such as angiotensin II and vasopressin, but not by autoregulation and the autonomic nervous system. It is known that the normal musculoelastic tissue in the vessel wall of the coiled artery, which supplies blood to the uteroplacental blood pool, is replaced by fibrinous tissue with advancing gestation. Therefore uteroplacental circulation is similar to arterio-venous shunt; it is possibly important for the homeostasis of maternal blood pressure. It is known that hypoxemia results in both the redistribution of feto-placental blood flow, the increase of blood flow in the placenta, and the increase of fetal vasoactive peptides. Since placental proteases (vasopressinase and angiotensinase) degrade vasoactive peptides, placental proteases protect the placental vessels from the vasoconstriction by vasoactive peptides and might contribute to the redistribution of feto-placental blood flow. Therefore placental proteases effect on fetal blood pressure via regulation of fetal vasoactive peptides, which regulate placental blood flow. Although human and animal pregnancy is normally associated with a refractory response to the pressor effect of exogenously infused angiotensin II, patients with pre-eclampsia as well as nonpregnant women are sensitive to angiotensin II; thin phenomenon has been studied as one of the causes of pre-eclampsia. Since the administration of placental angiotensinase was effective in lowering blood pressure in rats with hypertension induced by the infusion of angiotensin II, placental proteases are possibly involved in the refractory response to exogenously infused angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Angiotensin II; Animals; Blood Pressure; Cystinyl Aminopeptidase; Endopeptidases; Female; Fetus; Humans; Maternal-Fetal Exchange; Placenta; Pre-Eclampsia; Pregnancy; Rats; Vasopressins

Preeclampsia is characterized by increased vascular sensitivity to Angiotensin II, endothelial damage, and arteriolar spasm. We hypothesize that these events may be initiated by stimulation of V1 receptors. V1 receptors are normally activated by vasopressin. However, V1 receptors may be activated by the nonapeptide formed when vasopressin is metabolized by the placental enzyme--vasopressinase. This enzyme, found only in humans, cleaves the ring structure of vasopressin, but leaves the N-terminal end, the locus of pressor activity, intact. The resulting molecule, vasopressinase altered vasopressin (VAV), may be present in greater concentration in preeclamptic women and over the months of the second trimester initiate the cascade of pathophysiologic changes resulting in toxemia.

Topics: Cystinyl Aminopeptidase; Epidemiologic Factors; Female; Humans; Models, Biological; Pre-Eclampsia; Pregnancy; Vasopressins

To assess the value of cord plasma arginine vasopressin (AVP), erythropoietin (EP), and hypoxanthine (HX) as indices of asphyxia, we studied 62 infants of mothers with preeclampsia, 34 acutely asphyxiated infants, with 5-min Apgar score less than or equal to 6 and/or umbilical arterial pH less than or equal to 7.05, and 38 control infants. Umbilical arterial AVP in the asphyxia group (geometric mean; 95% confidence interval: 180; 92-350 pg/ml) was higher than in the control group (23; 8-66, p = 0.002) and correlated with umbilical arterial pH (r = -0.447, p = 0.028). AVP levels in the preeclampsia group did not differ from controls. Cord venous EP was higher in infants delivered by elective cesarean section from women with severe preeclampsia (115; 75-177 mU/ml, p less than 0.001) than in control infants (23; 18-27); in the whole group EP correlated with pH (r = -0.493, p less than 0.001). EP in the asphyxia group was similar (46; 35-65) to controls (40; 33-47) and did not correlate with pH. Cord arterial HX in the preeclampsia group was similar to controls (12.3; 9.5-16.0 mumol/liter), but elevated in the asphyxia group (23.7; 17.6-31.8, p = 0.001), in which HX correlated with pH (r = 0.558, p = 0.008) and AVP (r = 0.588, p = 0.005). EP did not correlate with AVP or HX in any group, nor did any of the variables correlate with the Apgar score. We conclude that cord plasma AVP and HX reflect acute asphyxia, whereas EP is elevated after more prolonged hypoxia.

Topics: Apgar Score; Asphyxia Neonatorum; Erythropoietin; Female; Fetal Blood; Humans; Hydrogen-Ion Concentration; Hypoxanthine; Hypoxanthines; Infant, Newborn; Male; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Female; Humans; Immersion; Molecular Weight; Pre-Eclampsia; Pregnancy; Temperature; Time Factors; Vasopressins

In 12 healthy pregnant women, 14 women with mild or moderate late pregnancy gestosis (EPH) and in 12 non-pregnant women, the influence of head out water immersion (WI) on mean blood pressure (MAP), the renin-aldosterone system, vasopressin (AVP) and atrial natriuretic hormone (ANF) was examined. WI induced a prompt fall in MAP in all examined groups. This decrease of MAP was maximal after 1 h WI, showing a tendency to rise later on in pregnant women. Simultaneously a decrease of plasma renin activity (PRA), plasma aldosterone, AVP and an increase of ANF was noted. The WI induced endocrine reaction pattern was qualitatively similar, but quantitatively different in the examined groups. In contrast to the response of non-pregnant women, healthy pregnant women and women with EPH gestosis showed a significantly smaller increase in ANF secretion induced by WI. No correlation was found between PRA, plasma AVP, aldosterone and ANF respectively. In addition changes in PRA, aldosterone, AVP and ANF did not correlate with WI-induced changes in MAP. From data obtained in this paper it seems, that WI-induced MAP changes are not related significantly to changes of the above mentioned hormonal factors.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Female; Humans; Hydrotherapy; Pre-Eclampsia; Pregnancy; Renin-Angiotensin System; Vasopressins

Decreased free water excretion and the development of interstitial edema are recognized characteristics of preeclampsia. However, the pathophysiology of decreased urine excretion in preeclampsia is presently controversial: diminished glomerular filtration, renal arteriolar spasm, elevated plasma vasopressin levels, and plasma volume contraction have been suggested as etiologies. We studied seven pregnant patients with a diagnosis of mild preeclampsia to assess the role of vasopressin, serum protein, and glomerular function in the renal excretion of water. The ability to excrete a water load was significantly and directly correlated with serum albumin (P less than 0.05) and protein (P less than 0.02) concentrations. Neither plasma vasopressin nor creatinine clearance correlated with water excretion. The similarity of preeclampsia and the nephrotic syndrome with regard to the renal excretion of water is discussed.

Topics: Anuria; Edema; Female; Glomerular Filtration Rate; Humans; Nephrotic Syndrome; Oliguria; Pre-Eclampsia; Pregnancy; Vasopressins; Water

The coexistence of diabetes insipidus and pregnancy is uncommon and can be associated with worsening of the diabetes insipidus. We report a patient who developed a transient nephrogenic diabetes insipidus associated with a pregnancy complicated by preeclampsia. The diabetes insipidus resolved spontaneously within several days after delivery.

Topics: Adult; Diabetes Insipidus; Female; Humans; Kidney Concentrating Ability; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Vasopressins

The maternal serum concentration of antidiuretic hormone (ADH) in a pregnancy uncomplicated by preeclampsia is identical to the ADH concentration in the nonpregnant female and normal male. However, elevated maternal ADH secondary to fetal hypothalamic ADH production and a genetic defect in maternal vasopressinase may be a cause of preeclampsia.

Topics: Chorionic Gonadotropin; Female; Humans; Hydatidiform Mole; Male; Pre-Eclampsia; Pregnancy; Seizures; Vasopressins

Cord plasma vasopressin concentration, determined by radioimmunoassay, was higher in arterial than in venous blood in 122 (84%) infants; the highest vasopressin values were recorded in 21 acidotic infants (mean cord pH, 7.13) delivered per vaginam and the lowest values in 50 infants delivered by cesarean section. Cord vasopressin levels were not elevated in infants delivered by cesarean section because of obstructed labor. There was a lack of correlation between vasopressin levels and the length of labor or cervical dilatation; a significant correlation was found between cord arterial vasopressin values and pH. Low vasopressin values were recorded in a group of 22 healthy infants (mean cord pH, 7.29) delivered by low forceps operation.

Topics: Abruptio Placentae; Adolescent; Adult; Cesarean Section; Delivery, Obstetric; Female; Fetal Growth Retardation; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Infant, Premature; Labor, Induced; Obstetrical Forceps; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Radioimmunoassay; Umbilical Cord; Vasopressins

The coexistence of diabetes insipidus (D.I.) and pregnancy is rare. Sixty-seven cases are reviewed, including one of our own. The condition tends to become worse in pregnancy, labor appears unaffected and lactation appears to lead to an improvement in D.I. Theories are discussed to account for the effect of pregnancy on D.I.

Topics: Adult; Diabetes Insipidus; Female; Humans; Labor, Obstetric; Lactation; Pre-Eclampsia; Pregnancy; Pregnancy in Diabetics; Vasopressins

Topics: Angiotensin II; Arm; Arteries; Autonomic Nervous System; Blood Pressure; Blood Viscosity; Blood Volume; Brain; Cardiac Output; Cardiovascular Physiological Phenomena; Cerebrovascular Circulation; Epinephrine; Female; Humans; Hypertension; Kidney; Leg; Liver Circulation; Norepinephrine; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Regional Blood Flow; Uterus; Vascular Resistance; Vasopressins

Topics: Aldosterone; Angiotensin II; Female; Humans; Pre-Eclampsia; Pregnancy; Renin; Sodium; Uric Acid; Vasopressins; Water

Topics: Adult; Anuria; Female; Humans; Nephrosis; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Blood Coagulation; Eclampsia; Female; Humans; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Adult; Clomiphene; Diabetes Insipidus; Ergonovine; Female; Humans; Infertility, Female; Labor, Induced; Ovulation; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Vasopressins

Topics: Adult; Animals; Catecholamines; Female; Humans; Kidney; Pre-Eclampsia; Pregnancy; Rabbits; Reflex; Uterus; Vasopressins

Topics: Adult; Aldosterone; Animals; Female; Gestational Age; Humans; Kidney; Potassium; Pre-Eclampsia; Pregnancy; Pregnancy, Animal; Rats; Reflex; Sodium; Time Factors; Uterus; Vasopressins

Topics: Adult; Female; Humans; In Vitro Techniques; Lysine; Placenta; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Amphetamine; Amyl Nitrite; Atropine; Edema; Female; Humans; Liver Diseases; Myxedema; Pre-Eclampsia; Pregnancy; Premenstrual Syndrome; Sodium Chloride; Vasopressins

Topics: Blood; Chemical Phenomena; Chemistry; Cystinyl Aminopeptidase; Female; Humans; Oxytocin; Peptide Hydrolases; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Blood Pressure; Body Weight; Diuresis; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Inulin; Kidney; Kidney Function Tests; Nephrosclerosis; Osmolar Concentration; Pathology; Pharmacology; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Vasopressins

Topics: Arginine Vasopressin; Blood Proteins; Enzymes; Female; Humans; Placental Extracts; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Female; Humans; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Arginine Vasopressin; Deamino Arginine Vasopressin; Female; Humans; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Female; Hormones; Pituitary Gland; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Arginine Vasopressin; Deamino Arginine Vasopressin; Female; Pre-Eclampsia; Pregnancy; Research; Vasopressins

Topics: Female; Peptides; Pre-Eclampsia; Pregnancy; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Female; Humans; In Vitro Techniques; Pre-Eclampsia; Pregnancy; Serum; Vasopressins

Topics: Arginine Vasopressin; Female; Humans; Pre-Eclampsia; Pregnancy; Sepsis; Toxemia; Vasopressins