Features of microvasculature regulation in patients with chronic kidney disease on peritoneal dialysis

Abstract

Introduction and aim. Chronic kidney disease (CKD) is one of the most common non-infectious diseases, in which arterial hypertension (AH) is progressing. The mechanisms of AH in CKD are complex and understudied. This research was conducted with the objective to investigate the mechanisms of microvascular tonus increase in the group of patients with the 5th stage of CKD who were treated with peritoneal dialysis. Materials and methods. Patients from dialysis department were included in the study (76 people). Blood flow in microvessels was measured by laser Doppler flowmetry (LDF). Results of LDF used for the calculation of neurogenic (HT), myogenic (MT) and endothelium-dependent tonus (EDT) microvessels. Cardiotonic steroid concentration in plasma was measured by competitive immunofluorescence using antibodies to ouabain and marinobufagenin. The activity of Na/K-ATPase was measured by spectrophotometry. Results and discussion. HT microvessels in patients with CKD was increased by 21.4±3,88 %, MT - 33.4±5,62 %, EDT 17.1±3.14 % compared with the control group. Endogenous ouabain (EO) concentration in plasma of patients with CKD was on average 0.311±0.032 nM/L, in the control - 0.296±0.031 nM/L. Marinobufagenin (MBG) concentration in the plasma of patients with CKD was 2.10; 0.89; 3.07 nM/L (median, 25th and 75th percentile), and in control - 0.347; 0.103; 0.427 nM/L. The activity of Na/K-ATPase in patients with CKD was 1.54±0.18 μmol Pi/mL/hr, vs. 3.07±0.44 μmol Pi/mL/h in the control. The correlation between the value of MT of microvascular and MBG concentration in blood plasma of patients with CKD was found (rs = 0.736). Conclusions. Our results show that high NT of microvessels of patients with CKD and is connected with increased activity of the central structures of the sympathetic nervous system, while increase of EDT is connected with endothelial dysfunction and increase of MT is connected with increasing concentration of MBG (not EO) in blood plasma. We believe that the MBG causes contraction of smooth muscle cells of blood vessels by activating signaling function of Na/K-ATPase.