Modeling renal autoregulation in a hemodynamic, first-trimester gestational model.

The maternal cardiovascular system, led by renal volume regulatory responses, changes during pregnancy to ensure an adequate circulation for fetal development and growth. Circulatory maladjustment predisposes to hypertensive complications during pregnancy. Mathematical models can be used to gain insight in the gestational cardiovascular physiology. In this study, we developed an accurate, robust, and transparent model for renal autoregulation implemented in an existing circulatory gestational model. This renal autoregulation model aims to maintain steady glomerular pressure by the myogenic response, and glomerular filtration rate by tubuloglomerular feedback, both by inducing a change in the radius, and thus resistance, of the afferent arteriole. The modeled response of renal blood flow and the afferent arteriole following blood pressure increase were compared to published observations in rats. With solely the myogenic response, our model had a maximum deviation of 7% in change in renal blood flow and 7% in renal vascular resistance. When both the myogenic response and tubuloglomerular feedback were concurrently activated, the maximum deviation was 7% in change in renal blood flow and 5% in renal vascular resistance. These results show that our model is able to represent renal autoregulatory behavior comparable to empirical data. Further studies should focus on extending the model with other regulatory mechanisms to understand the hemodynamic changes in healthy and complicated pregnancy.