Inflammatory state, blood pressure and progression of vascular wall injury in experimental chronic kidney disease

Background The inflammation is a well-documented factor influencing the development of cardiovascular complications in chronic kidney disease (CKD) and hypertension. The aim of this study was to examine systemic inflammatory state defined by level of serum haptoglobin, local inflammation defined by monocyte chemotactic protein (MCP-1) level, blood pressure and arterial response to phenylephrine (PHE) and angiotensin II (ANG II) in a different stages of renal failure. Material and methods Experiments were performed on male Wistar rats, weighing 290-380 g. The rats were divided into four groups: I (control) - shame-operated (n = 12), II - 1/2 nephrectomy (n = 12), III - 3/4 nephrectomy (n = 8), IV - 5/6 nephrectomy (n = 12). After 4 weeks blood pressure (BP) in carotid artery was measured and the blood was collected for BUN, creatinine, albumin, haptoglobin and MCP-1. Then we compared the smooth muscle contractility of rat tail artery after stimulation with PHE and ANG II in all groups. The constriction of artery was measured as an increase in perfusion pressure at a constant flow of the perfusion fluid. Cumulative response curves (CRCs) were obtained using van Rossum method. Results We observed the increased arterial reaction to agonists in the first stages of renal failure (PHE: group II, III; ANG II: group II) and diminished vasoconstruction reaction in 5/6 nephrectomy. Systemic inflammation defined by haptoglobin level occured in 1/2 nephrectomy group and did not increase in more advanced stages of renal disease. The local inflammation (MCP-1-level) increased in paralel to the renal failure progression. Conclusions The inflammatory state plays a key role in determining of vascular contraction and resistant artery tone.