LONGITUDINAL STUDY OF VOLUME EXPANSION IN HEALTHY PREGNANT WOMEN

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Chronic hypertension is maintained by different mechanisms including: (1) arterial overfilling (volume-dependent hypertension); (2) arterial constriction without increased volume (vasoconstrictive hypertension) ; or (3) a combination of both. The kidneys play a key role by sustaining sodium and volume in excess of vascular capacity despite increases in renal perfusion pressure. It is estimated that 30-40% of patients have a volume-dependent form of hypertension. Under normal conditions, volume expansion as well as parathyroid hormone (PTH) cause decreased resorption of sodium and phosphate in the proximal convoluted tubule of the kidney. Acutely, this rejection of sodium and phosphate may be due to phosphorylation of a proximal tubule brush border protein (related to the sodium/phosphorus co-transporter). In animal models of volume expansion hypertension, the phosphorylation of this protein is down-regulated in chronic hypertension. Contrastingly, in animal models of vasoconstrictive hypertension, the phosphorylation of this protein is maintained. Normal pregnancy is a state of volume expansion. For this reason, this study will aim to evaluate longitudinally in healthy pregnant women a recently characterized proximal renal tubular brush border protein thought to regulate volume. Pregnant women provide an opportunity to study changes in quantity and phosphorylation of the regulatory protein in a normal physiologic state of changing volume. This information will aid in understanding the regulator protein in some forms of hypertension.