Serial Estimation of Plasma Renin Concentration During Pregnancy and After Parturition

Brown, Jerry M.; Davies, David; Doak, P. B.; Lever, A. F.; Robertson, J. I. S.

doi:10.1677/joe.0.0350373

Cited by 39 publications

(10 citation statements)

References 19 publications

(30 reference statements)

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“…A similar wide variability in PRA has been described in pregnant dogs (17) and humans (18). Differences in substrate concentration known to be elevated with pregnancy might in part account for the variability.…”

Section: Methodssupporting

confidence: 59%

Uterine blood flow and uterine renin secretion

Ferris¹,

Stein²,

Kauffman³

1972

J. Clin. Invest.

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Section: Methodssupporting

confidence: 59%

Uterine blood flow and uterine renin secretion

Ferris¹,

Stein²,

Kauffman³

1972

J. Clin. Invest.

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“…The enzyme can be found in amniotic fluid (37) and will form angiotensin II (38), but apparently does not respond to the same physiologic stimuli, i.e., salt loading and hypervolemia, that suppress renal renin production (39,40). This could provide another possible sustained stimulus to aldosterone production in pregnancy.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Estradiol and Estriol on Plasma Levels of Cortisol and Thyroid Hormone-Binding Globulins and on Aldosterone and Cortisol Secretion Rates in Man*

Katz¹,

Kappas²

1967

J. Clin. Invest.

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Summary. The effects of estriol and estradiol on the plasma levels of cortisol-and thyroxine-binding globulin activity, and on the secretion rates of aldosterone and cortisol were studied in man. The metabolite estriol had no consistent or significant influence on plasma levels of the hormone-binding globulin activities; the hormone estradiol increased these binding capacities significantly, as expected. Cortisol secretion rate rose slightly after estriol but was unchanged after estradiol. Both compounds induced substantial increases in the aldosterone secretion-rate of most treated subjects. The mechanism of this apparently paradoxical effect of estrogens is not clear; it is suggested that the "salt-retaining" action of estrogens is mediated in part by the rapid enhancement of aldosterone output which follows their administration in man. Balance experiments in four subjects suggest that both estradiol and estriol may induce a transient early natriuresis in man; but other mechanisms for estrogen stimulation of aldosterone secretion may be operative as well. IntroductionEstriol is quantitatively the most important metabolite of estradiol, being derived from this hormone and related precursors such as estrone, via a chemical transformation which is not reversible in vivo (1). Its production is known to increase extraordinarily in pregnancy, reaching levels of

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“…Normal human pregnancy, compared to the nonpregnant state, is characterized by increased plasma renin concentration, renin activity, renin substrate, angiotensin II (A-II),' and aldosterone (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Elevated excretory and secretory rates of aldosterone also have been observed in normal pregnancy (12)(13)(14)(15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

Gant¹,

et al. 1973

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A B S T R A C T The present study was designed to ascertain sequentially the pressor response to angiotensin II in young primigravid patients throughout pregnancy in order a) to define when in pregnancy resistance to the pressor effects of angiotensin II develops; b) to define the physiologic sequence of events leading to this resistance; and c) to ascertain whether sensitivity to infused angiotensin II could be detected before the onset of clinical signs of pregnancy-induced hypertension.With this prospective approach, two separate groups of patients were defined. The first group of patients remained normal throughout pregnancy. The second group consisted of those patients who, while clinically normotensive during the initial phase of the study, ultimately developed hypertension of pregnancy.192 patients were studied; of these, 120 patients remained normotensive and 72 developed pregnancy-induced hypertension. In both groups, vascular resistance to infused angiotensin II (more than 8 ng/kg/min required to elicit a pressor response of 20 mm Hg in diastolic pressure) was demonstrated as early as the 10th wk of pregnancy. In the group that remained normotensive, maximum mean vascular resistance occurred at 18-30 wk of pregnancy, (mean pressor dose required being 13.5 to 14.9 ng/kg/min). In those subjects who developed pregnancy-induced hypertension, the mean maximum dose required was 12.9 ng/kg/min, which was observed at the 18th wk of pregnancy. By the 22nd wk there was a clear separation of the two groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the two groups became significant (P < 0.01) by [23][24][25][26]

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Serial Estimation of Plasma Renin Concentration During Pregnancy and After Parturition

Cited by 39 publications

References 19 publications

Uterine blood flow and uterine renin secretion

Uterine blood flow and uterine renin secretion

The Effects of Estradiol and Estriol on Plasma Levels of Cortisol and Thyroid Hormone-Binding Globulins and on Aldosterone and Cortisol Secretion Rates in Man*

A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

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