Functional activity of blood cells in chronic obstructive pyelonephritis

Objective. Evaluation of the involvement of a-, P-adrenoreceptors and purine P2-receptors in the formation of leukocyte-platelet aggregates (LPA) in patients with chronic obstructive pyelonephritis (COPN). Material and methods. The study included 43 patients with COPN, whose diagnosis was verified on the basis of complaints, medical history, physical examination, results of clinical, laboratory and instrumental tests. 26 patients were examined during COPN remission, 17 patients - during exacerbation phase. The formation of LPA was modeled in vitro by adding agonists at the final dose of EC50 to the peripheral blood. Adrenaline, adenosine diphosphate (ADP) and platelet activating factor (PAF) were used as blood cell receptor agonists. Results. In COPN remission (chronic urinary tract inflammation), paracrine stimulation of platelets with active leukocytes in the process of LPA formation reproduced a more pronounced effect than the systemic mechanism that ensures the activation of leukocytes and platelates with adrenaline. Activation of the sympathoadrenal system in urolithiasis can be a risk factor for COPN exacerbation, since adrenaline can stimulate platelates, which will modulate the functional activity of leukocytes in this case. In COPN exacerbation (acute inflammatory reaction in urinary tract), activation of platelet PAF-receptors with the participation of leukocytes is more effective in terms of the formation of LPA than stimulation of leukocyte P2Y-receptors with purines (ATP and ADP) secreted from dense granules of platelets. The systemic mechanism of blood cell activation is manifested by the predominant involvement of leukocytes in the implementation of the inflammatory reaction, which can stimulate platelets. In turn, the platelets secreting ADP activate the purine receptors of leukocytes, thereby increasing the effect of adrenaline on leukocytes (amplifying the signal from the a-ADRENORECEPTOR). Conclusion. In the phase of remission and exacerbation cop, the formation of LPA and the recruitment of blood leukocytes from circulating blood to the inflammatory focus are achieved by including systemic (influence of adrenaline) and paracrine mechanisms (secretion of ATP, ADP and PAF). The effect achieved depends on the activity of the a2-, p2-adrenergic receptors, P2Y-purine and vat platelet receptors and leukocytes.

leukocyte-platelet aggregates, regulation of inflammation, PAF