Hypertensive and Normal Pregnancy--Calcium Metabolism and Renin-Angiotensin - SCOR in Hypertension
|First Received Date ICMJE||May 25, 2000|
|Last Updated Date||June 23, 2005|
|Start Date ICMJE||December 1990|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures ICMJE||Not Provided|
|Original Primary Outcome Measures ICMJE||Not Provided|
|Change History||Complete list of historical versions of study NCT00005456 on ClinicalTrials.gov Archive Site|
|Current Secondary Outcome Measures ICMJE||Not Provided|
|Original Secondary Outcome Measures ICMJE||Not Provided|
|Current Other Outcome Measures ICMJE||Not Provided|
|Original Other Outcome Measures ICMJE||Not Provided|
|Brief Title ICMJE||Hypertensive and Normal Pregnancy--Calcium Metabolism and Renin-Angiotensin - SCOR in Hypertension|
|Official Title ICMJE||Not Provided|
To study calcium metabolism and the renin-angiotensin system in hypertensive and normal pregnancy.
Beginning in Fiscal Year 1975, the multidisciplinary SCOR examined causes, consequences, and treatments of human hypertension. A central theme was the renal basis for human hypertension. The subproject on calcium metabolism and the renin-angiotensin system in hypertensive and normal pregnancy began in December, 1990.
A longitudinal study was performed on normal pregnant women and women with chronic hypertension who had a high incidence of superimposed preeclampsia. In a previous study, the investigators had demonstrated that preeclampsia was associated with reduced urinary excretion of calcium and with lower plasma renin activity (PRA) compared with normal pregnancy. The goal of the investigators was to identify the metabolic and cellular basis for these alterations in calcium homeostasis and in the renin angiotensin system. They tested two hypotheses. The first hypothesis was that diminished placental and/or renal production of 1,25-dihydroxyvitamin D, leading to lower serum calcium, higher parathyroid hormone, and increased renal tubular reabsorption of calcium, was the metabolic basis for hypocalciuria in preeclampsia. The second hypothesis was that lower PRA in preeclampsia was due to systemic and renal vasoconstriction with hypertension and diminished natriuresis.
Serial measurements of 1,25-dihydroxyvitamin D, parathyroid hormone, serum ionized calcium, PRA, estradiol and progesterone, and urinary calcium and electrolytes were obtained, particularly at the onset of preeclampsia. Acute renal hemodynamic studies were also performed in women with preeclampsia and in gestational age matched normals. The studies investigated the relationships among glomerular filtration rate, renal blood flow, parathyroid hormone, vitamin D, atrial natriuretic factor, renin, estradiol and progesterone, and sodium and calcium excretion during infusion of inulin and PAH with either saline or calcium chloride.
Intracellular free calcium concentration in platelets and lymphocytes of pregnant women participating in longitudinal and acute renal hemodynamic studies were also measured. Basal and stimulated (with angiotensin II, ionomycin and thrombin), intracellular free calcium concentrations were compared in normal and hypertensive pregnant women and correlated with calcium regulatory hormones, plasma renin activity and hypertension.
|Study Type ICMJE||Observational|
|Study Design ICMJE||Observational Model: Natural History
Time Perspective: Longitudinal
|Target Follow-Up Duration||Not Provided|
|Sampling Method||Not Provided|
|Study Population||Not Provided|
|Intervention ICMJE||Not Provided|
|Study Group/Cohort (s)||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Recruitment Status ICMJE||Completed|
|Enrollment ICMJE||Not Provided|
|Completion Date||November 1995|
|Primary Completion Date||Not Provided|
|Eligibility Criteria ICMJE||
No eligibility criteria
|Accepts Healthy Volunteers||No|
|Contacts ICMJE||Contact information is only displayed when the study is recruiting subjects|
|Location Countries ICMJE||Not Provided|
|NCT Number ICMJE||NCT00005456|
|Other Study ID Numbers ICMJE||4900|
|Has Data Monitoring Committee||Not Provided|
|Responsible Party||Not Provided|
|Study Sponsor ICMJE||National Heart, Lung, and Blood Institute (NHLBI)|
|Collaborators ICMJE||Not Provided|
|Information Provided By||National Heart, Lung, and Blood Institute (NHLBI)|
|Verification Date||March 2005|
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP