Hypertension in end-stage renal disease Manuel Martínez-Maldonado  Kidney International  Volume 54, Pages S67-S72 (December 1998) DOI: 10.1046/j.1523-1755.1998.06816.x Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 1 Factors that may alter cardiac output and total peripheral resistance in end-stage renal disease, and thus raise blood pressure. The role of abnormal channel function is hypothetical, but it might contribute to either an increase in peripheral resistance or an increase in cardiac output (detailed in the text and Figure 3). Kidney International 1998 54, S67-S72DOI: (10.1046/j.1523-1755.1998.06816.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 2 Sequential response to volume expansion in anephric patients and those with renal disease: the theory of whole-body autoregulation18. Kidney International 1998 54, S67-S72DOI: (10.1046/j.1523-1755.1998.06816.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 3 Different responses to salt and water loading leading to hypertension in anephric and ESRD patients19. Kidney International 1998 54, S67-S72DOI: (10.1046/j.1523-1755.1998.06816.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 4 Endothelin-1 (ET-1) can contribute to hypertension in several ways. In this hypothetical proposal by Markewitz and Kohan34, it is suggested that the development of excessive responsiveness to the peptide may arise from either an increased number of receptor or a decreased intrarenal degradation of ET-1. It is unclear if the kidney secretes ET-1 into the circulation in chronic renal disease. Equally unclear is whether ET-1 is a cause of hypertension or if its high levels in ESRD represent endothelial injury induced by hypertension (see text). Paradoxically, the contribution of ET-1 to ESRD hypertension might include reversal of its effects on inner medullary collecting duct (IMCD) to inhibit sodium and water reabsorption. This could result from an alteraltion in receptor number or sensitivity induced by the chronic disease state effect on the IMCD. Kidney International 1998 54, S67-S72DOI: (10.1046/j.1523-1755.1998.06816.x) Copyright © 1998 International Society of Nephrology Terms and Conditions