Ouabain-Like Na+, K+-ATPase Inhibitory Activity of a Plasma Extract in Normal Pregnancy and Pregnancy Induced Hypertension

1. Active plasma renin concentration but not total renin concentration is reduced in women with pregnancy-induced hypertension compared with normotensive pregnant women. This study was conducted to determine whether women with pregnancy-induced hypertension are able to stimulate release of active renin. 2. Active plasma renin concentration was measured as the generation of angiotensin I at physiological pH in the presence of excess renin substrate, and total renin concentration was determined in the same way after trypsin activation. Inactive plasma renin concentration was calculated as the difference between total renin and active plasma renin concentrations. 3. Resting active plasma renin concentration was significantly greater in third-trimester primigravidae compared with normotensive non-pregnant women and active plasma renin and total renin concentrations rose significantly without a fall in inactive plasma renin concentration in both groups after 2 h ambulation, suggesting increased release of active plasma renin and not conversion of circulating inactive to active renin. These responses were blunted in women taking oral contraceptives. 4. Although the active plasma renin concentration was significantly reduced in third-trimester primigravidae with pregnancy-induced hypertension, total renin concentration was not significantly different compared with normotensive women of similar gestation and in both groups 30 min 60° head-up tilt increased active but not inactive plasma renin concentration. 5. These studies show that in normal pregnancy active plasma renin concentration can be stimulated to a similar extent as in non-pregnant women, despite a higher resting level. This appears to be due to increased secretion of active plasma renin rather than conversion of circulating inactive to active renin. Women with pregnancy-induced hypertension are also still able to stimulate secretion of active renin despite resting concentrations similar to those of non-pregnant women. These data suggest that in pregnancy-induced hypertension basal secretion of active renin is prematurely reset to that in the non-pregnant state but that secretion of active renin responds normally to posture.

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Urinary Albumin Excretion in Normal Pregnancy and Pregnancy-Induced Hypertension

Nephron ◽

10.1159/000186601 ◽

1991 ◽

Vol 59 (3) ◽

pp. 416-422 ◽

Cited By ~ 25

Author(s):

Rocco Misiani ◽

Donatella Marchesi ◽

Giacomo Tiraboschi ◽

Lucio Gualanãris ◽

Roberto Pagnf ◽

...

Keyword(s):

Urinary Albumin Excretion ◽

Normal Pregnancy ◽

Urinary Albumin ◽

Pregnancy Induced Hypertension ◽

Albumin Excretion ◽

Induced Hypertension

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Plasma beta-thromboglobulin in normal pregnancy and pregnancy-induced hypertension

European Journal of Obstetrics & Gynecology and Reproductive Biology ◽

10.1016/0028-2243(83)90262-9 ◽

1983 ◽

Vol 14 (4) ◽

pp. 209-216 ◽

Cited By ~ 9

Author(s):

J.I.P. de Vries ◽

E. Vellenga ◽

J.G. Aarnoudse

Keyword(s):

Normal Pregnancy ◽

Pregnancy Induced Hypertension ◽

Induced Hypertension

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Soluble Fas and Fas Ligand in Pregnancy

Angiology ◽

10.1177/0003319711406901 ◽

2011 ◽

Vol 63 (1) ◽

pp. 35-38 ◽

Cited By ~ 5

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.

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

Clinical Science ◽

10.1042/cs0850063 ◽

1993 ◽

Vol 85 (1) ◽

pp. 63-70 ◽

Cited By ~ 3

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.

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