The maintenance of a normal pregnancy requires significant and sustained plasma volume expansion. In normotensive pregnant rats, the process is achieved by significant attenuation of pressure natriuresis and diuresis. Relaxin is a peptide hormone that has been traditionally associated with pregnancy in mammals. Increasing evidence suggests that relaxin plays a role in the systemic hemodynamic changes of pregnancy, including the generalized vasodilation. Relaxin reduces fibrosis in the kidney, heart, and lung and significantly decreases the total collagen content in non-pregnant female Sprague-Dawley (SD) rats. Also, nitric oxide (NO), which is a vasodilator, is increased during normal pregnancy. Based on these established effects of relaxin and NO, it is reasonable to suggest that relaxin, NO, as well as other factors that are increased or activated during pregnancy may play an important role in the increase in renal interstitial compliance (∆ in renal interstitial volume/∆ in renal interstitial hydrostatic pressure) and renal sodium handling during pregnancy.
Therefore, we propose to investigate the role of relaxin on affecting various transporters in Human Renal Proximal Tubule Epithelial Cells (RPTEC). The possible interaction between relaxin and NO on these transporters will be determined in RPTEC.
The objective of this project is to determine the specific effects of relaxin and NO on the activity of proximal tubule transporters Na+-K+-ATPase and sodium hydrogen exchanger-3 (NHE-3) in RPTEC.