Blood Pressure Patterns in Normal Pregnancy and in Pregnancy-Induced Hypertension, Preeclampsia, and Chronic Hypertension

1996 ◽  
Vol 88 (4) ◽  
pp. 503-510 ◽  
Author(s):  
C BENEDETTO
Keyword(s):  
Blood Pressure ◽  
Normal Pregnancy ◽  
Chronic Hypertension ◽  
Pregnancy Induced Hypertension ◽  
Induced Hypertension ◽  
Blood Pressure Patterns ◽  
In Pregnancy

scholarly journals Normal pregnancy: mechanisms underlying the paradox of a ouabain-resistant state with elevated endogenous ouabain, suppressed arterial sodium calcium exchange, and low blood pressure

2012 ◽  
Vol 302 (6) ◽  
pp. H1317-H1329 ◽  
Author(s):  
Brandiese E. Jacobs ◽  
Yong Liu ◽  
Maria V. Pulina ◽  
Vera A. Golovina ◽  
John M. Hamlyn
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Normal Pregnancy ◽  
Pregnancy Induced Hypertension ◽  
Sodium Calcium ◽  
Endogenous Ouabain ◽  
Induced Hypertension ◽  
Calcium Exchange ◽  
Resistant State ◽  
In Pregnancy

Endogenous cardiotonic steroids (CTS) raise blood pressure (BP) via vascular sodium calcium exchange (NCX1.3) and transient receptor-operated channels (TRPCs). Circulating CTS are superelevated in pregnancy-induced hypertension and preeclampsia. However, their significance in normal pregnancy, where BP is low, is paradoxical. Here we test the hypothesis that vascular resistance to endogenous ouabain (EO) develops in normal pregnancy and is mediated by reduced expression of NCX1.3 and TRPCs. We determined plasma and adrenal levels of EO and the impact of exogenous ouabain in pregnancy on arterial expression of Na+ pumps, NCX1.3, TRPC3, and TRPC6 and BP. Pregnant (embryonic day 4) and nonpregnant rats received infusions of ouabain or vehicle. At 14–16 days, tissues and plasma were collected for blotting and EO assay by radioimmunoassay (RIA), liquid chromatography (LC)-RIA, and LC-multidimensional mass spectrometry (MS3). BP (−8 mmHg; P < 0.05) and NCX1.3 expression fell (aorta −60% and mesenteric artery −30%; P < 0.001) in pregnancy while TRPC expression was unchanged. Circulating EO increased (1.14 ± 0.13 nM) vs. nonpregnant (0.6 ± 0.08 nM; P < 0.05) and was confirmed by LC-MS3 and LC-RIA. LC-MS3 revealed two previously unknown isomers of EO; one increased ∼90-fold in pregnancy. Adrenal EO but not isomers were increased in pregnancy. In nonpregnant rats, similar infusions of ouabain raised BP (+24 ± 3 mmHg; P < 0.001). In ouabain-infused rats, impaired fetal and placental growth occurred with no BP increase. In summary, normal pregnancy is an ouabain-resistant state associated with low BP, elevated circulating levels of EO, two novel steroidal EO isomers, and increased adrenal mass and EO content. Ouabain raises BP only in nonpregnant animals. Vascular resistance to the chronic pressor activity of endogenous and exogenous ouabain is mediated by suppressed NCX1.3 and reduced sensitivity of events downstream of Ca2+ entry. The mechanisms of EO resistance and the impaired fetal and placental growth due to elevated ouabain may be important in pregnancy-induced hypertension (PIH) and preeclampsia (PE).

Managing high blood pressure in pregnancy

1993 ◽  
Vol 31 (14) ◽  
pp. 53-56
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
High Blood Pressure ◽  
Chronic Hypertension ◽  
Pregnancy Induced Hypertension ◽  
Hypertension In Pregnancy ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
In Pregnancy

Raised arterial blood pressure is common in pregnancy. Usually it is due solely to the pregnancy and resolves within days or weeks of delivery (pregnancy-induced hypertension – PIH). Occasionally it is chronic hypertension which predates or begins during pregnancy; it persists after delivery. In some women it is a mixture of both, with pregnancy-induced hypertension superimposed on existing chronic hypertension. In this article we discuss the risks to mother and fetus of hypertension in pregnancy and review its prevention and management.

Soluble Fas and Fas Ligand in Pregnancy

Angiology ◽  
2011 ◽  
Vol 63 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Velore J. Karthikeyan ◽  
Gregory Y. H. Lip ◽  
Sabah Baghdadi ◽  
Deirdre A. Lane ◽  
D. Gareth Beevers ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Fas Ligand ◽  
Normal Pregnancy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pregnancy Induced Hypertension ◽  
Control Groups ◽  
Pregnancy Hypertension ◽  
Soluble Fas ◽  
Induced Hypertension ◽  
In Pregnancy

The pathophysiology of pregnancy-induced hypertension and preeclampsia may involve abnormalities in placentation and the Fas/Fas ligand system. Hypothesizing abnormal plasma Fas and Fas ligand in pregnancy-induced hypertension, we recruited 20 hypertensive pregnant women at mean week 15 and 29 at week 30: 18 were studied at both time points. Control groups were 20 normotensive pregnant women at week 20, 29 women at week 27, and 50 nonpregnant women. sFas and sFas ligand (sFasL) were measured by enzyme-linked immunosorbent assay (ELISA). The hypertensive women had lower sFasL at both stages of their pregnancy ( P < .05). There were no differences in sFas. In 18 hypertensive pregnant women, sFasL fell from week 15 to week 29 ( P < .03). We conclude that sFas and sFasL is unchanged in normal pregnancy. Hypertension in pregnancy is characterized by low sFasL, and levels fall from weeks 15 to 29. This may reflect differences in placentation in the differing physiological and pathological states.

Neutrophil Platelet-Activating Factor in Normal and Hypertensive Pregnancy and in Pregnancy-Induced Hypertension

1993 ◽  
Vol 85 (1) ◽  
pp. 63-70 ◽  
Author(s):  
L. J. Beilin ◽  
K. D. Croft ◽  
C. A. Michael ◽  
J. Ritchie ◽  
L. Schmidt ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Normal Pregnancy ◽  
Pregnancy Induced Hypertension ◽  
Uncomplicated Hypertension ◽  
Control Subjects ◽  
Significant Difference ◽  
Induced Hypertension ◽  
In Pregnancy

1. Platelet-activating factor is a phospholipid with potent vasodilator and platelet-activating properties. To test the hypothesis that a generalized change in cellular platelet-activating factor metabolism may be involved in the systemic vasodilatation of normal pregnancy or pregnancy-induced hypertension, we studied platelet-activating factor and eicosanoid synthesis in isolated leucocytes obtained from pregnant women before and after delivery compared with age-matched non-pregnant control subjects. Parallel observations were carried out in age- and gestation-matched women with uncomplicated hypertension in pregnancy and in women with pregnancy-induced hypertension and a further set of normotensive pregnant control subjects. 2. Leucocyte counts were higher in all pregnant groups compared with non-pregnant control subjects. Neutrophil production of platelet-activating factor and metabolites of prostacyclin, prostaglandin E2 and thromboxane in response to calcium ionophore stimulation were all lower in pregnant women compared with non-pregnant control subjects, but returned to similar levels 6 weeks post partum. There was no significant difference between essential hypertensive and normotensive groups. When women with pregnancy-induced hypertension were a priori subdivided into those with or without proteinuria, subjects with proteinuria showed significantly lower levels of neutrophil platelet-activating factor synthesis. 3. Plasma levels of the platelet-activating factor metabolite (lyso-platelet-activating factor) were also lower in pregnancy, suggesting alterations in the activity of enzymes controlling synthesis or degradation of this phospholipid in pregnancy. In pregnancy-induced hypertension the levels of plasma lyso-platelet-activating factor were higher than in normal pregnancy. 4. Thus this study demonstrates a reduction in the maximum capacity of neutrophils to synthesize platelet-activating factor and the three main classes of eicosanoids in vitro and a reduction in plasma lyso-platelet-activating factor levels in normotensive and essential hypertensive pregnancies. Contrary to expectation neutrophil prostacyclin metabolite generation was reduced in normal pregnancy. In pregnancy-induced hypertension with proteinuria the suppression of neutrophil platelet-activating factor synthesis was more pronounced. The results do not support the involvement of platelet-activating factor in the vasodilatation of pregnancy, but indicate profound changes in cellular phospholipid metabolism in normal pregnancy with further disturbances in pregnancy-induced hypertension by as yet unexplained mechanisms.

Plasma catecholamines in pregnancy induced hypertension

1986 ◽  
Vol 71 (1) ◽  
pp. 111-115 ◽  
Author(s):  
Peter C. Rubin ◽  
Lucy Butters ◽  
Rosemary McCabe ◽  
John L. Reed
Keyword(s):  
Blood Pressure ◽  
Post Partum ◽  
Plasma Concentrations ◽  
Plasma Noradrenaline ◽  
Pregnancy Induced Hypertension ◽  
Noradrenaline Concentration ◽  
Induced Hypertension ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline ◽  
In Pregnancy

1. Increased activity of the sympathetic nervous system has been implicated in the genesis of early hypertension in young people. Studies in pregnancy allow observations to be made on evolving, recently established and resolving hypertension in the human. We describe the results of two studies involving women who developed hypertension during pregnancy. 2. In the first study, plasma concentrations of noradrenaline and adrenaline were measured in 17 women with pregnancy induced hypertension (PIH) and 17 normotensive pregnant control subjects. Plasma noradrenaline (nmol/l) was lower in the PIH group compared with control patients in both semi-recumbent (1.11 ± 0.53 vs 1.98 ± 0.96, P < 0.001) and standing positions (1.31 ± 0.65 vs 2.57 ± 1.27, P < 0.005). Five days post partum, plasma noradrenaline had risen in the PIH group compared with pregnant values in semi-recumbent (1.65 ± 1.0 vs 1.11 ± 0.52, P < 0.05) and standing positions (2.46 ± 1.5 vs 1.31 ± 0.65, P < 0.05). In the normotensive patients plasma noradrenaline did not differ between post partum and pregnant values (1.51 ± 0.73 vs 1.98 ± 0.96 semi-recumbent; 2.00 ± 1.16 vs 2.57 ± 1.7 standing). 3. Logarithmic transformation of the noradrenaline concentration data resulted in a significant (P < 0.02) negative correlation with diastolic blood pressure in the pregnant patients but not post partum. Plasma adrenaline concentration was the same in both groups. 4. In the second study, plasma concentrations of noradrenaline and adrenaline were measured sequentially through pregnancy in five women who developed PIH and five control subjects who remained normotensive. There was no difference in catecholamine concentrations between groups at any stage, but noradrenaline concentration tended to fall as blood pressure rose in the PIH patients. 5. We conclude that the sympathetic nervous system does not contribute to the development of PIH but responds to the increased blood pressure with decreased activity.

A ouabain-displacing factor in normal pregnancy, pregnancy-induced hypertension and pre-eclampsia

1988 ◽  
Vol 74 (3) ◽  
pp. 307-310 ◽  
Author(s):  
I. Gregoire ◽  
D. Roth ◽  
G. Siegenthaler ◽  
P. Fievet ◽  
N. El Esper ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Receptor Binding ◽  
Adenosine Triphosphatase ◽  
Binding Assay ◽  
Normal Pregnancy ◽  
Pregnancy Induced Hypertension ◽  
Sodium Potassium ◽  
Receptor Binding Assay ◽  
Induced Hypertension ◽  
In Pregnancy

1. A ouabain-displacing factor (ODF) was measured in the urine of non-pregnant, normotensive pregnant and hypertensive pregnant women by a receptor-binding assay with sodium, potassium-dependent adenosine triphosphatase. 2. Urinary ODF was significantly increased in normal pregnancy. 3. Greater increases were seen in pregnancy-induced hypertension and pre-eclampsia.

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