Normotensive blood pressure in pregnancy – the role of salt and aldosterone

Gennari, Carine; Escher, Geneviève; Kramer, Simea; Dick, Bernhard; Eisele, Nicole; Baumann, Marc Ulrich; Raio, Luigi; Frey, Felix J.; Surbek, Daniel; Mohaupt, Markus (2014). Normotensive blood pressure in pregnancy – the role of salt and aldosterone. Hypertension, 63(2), pp. 362-368. Lippincott Williams & Wilkins 10.1161/HYPERTENSIONAHA.113.02320

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A successful pregnancy requires an accommodating environment. Salt and water availability are critical for plasma volume expansion. Any changes in sodium intake would alter aldosterone, a hormone previously described beneficial in pregnancy. To date, it remains ambiguous whether high aldosterone or high salt intake is preferable. We hypothesized that increased aldosterone is a rescue mechanism and appropriate salt availability is equally effective in maintaining a normotensive blood pressure (BP) phenotype in pregnancy. We compared normotensive pregnant women (n=31) throughout pregnancy with young healthy female individuals (n=31–62) and performed salt sensitivity testing within the first trimester. Suppression of urinary tetrahydro-aldosterone levels by salt intake as measured by gas chromatography–mass spectrometry and urinary sodium excretion corrected for creatinine, respectively, was shifted toward a higher salt intake in pregnancy (P<0.0001). In pregnancy, neither high urinary tetrahydro-aldosterone nor sodium excretion was correlated with higher BP. In contrast, in nonpregnant women, systolic BP rose with aldosterone (P<0.05). Testing the impact of salt on BP, we performed salt sensitivity testing in a final cohort of 19 pregnant and 24 nonpregnant women. On salt loading, 24-hour mean arterial pressure rose by 3.6±1.5 and dropped by –2.8±1.5 mm Hg favoring pregnant women (P<0.01; χ2=6.04; P<0.02). Our data suggest first that salt responsiveness of aldosterone is alleviated in conditions of pregnancy without causing aldosterone-induced hypertension. Second, salt seems to aid in BP lowering in pregnancy for reasons incompletely elucidated, yet involving renin suppression and potentially placental sensing mechanisms. Further research should identify susceptible individuals and clarify effector mechanisms.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Nephrology and Hypertension
04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Gynaecology
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > Unit Childrens Hospital > Forschungsgruppe Nephrologie / Hypertonie

UniBE Contributor:

Gennari, Carine; Escher, Geneviève; Dick, Bernhard; Eisele, Nicole; Baumann, Marc Ulrich; Raio, Luigi; Surbek, Daniel and Mohaupt, Markus

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0194-911X

Publisher:

Lippincott Williams & Wilkins

Language:

English

Submitter:

Markus Georg Mohaupt

Date Deposited:

16 Apr 2015 11:50

Last Modified:

25 Nov 2015 11:11

Publisher DOI:

10.1161/HYPERTENSIONAHA.113.02320

PubMed ID:

24296282

BORIS DOI:

10.7892/boris.66909

URI:

https://boris.unibe.ch/id/eprint/66909

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