[Uncontrolled Arterial Hypertension: Kidney, Neurohormonal Imbalance, and Approaches to Antihypertensive Drug Therapy].

Resistant and refractory arterial hypertensions are two distinct clinical phenotypes of uncontrolled arterial hypertension (AH), which differ in their sensitivity to antihypertensive drug therapy. The review presents data obtained in clinical studies devoted to elucidating the involvement of disorders of neurohormonal status and renal function in the formation of resistant and refractory arterial hypertension, to and the development of new approaches to increasing the effectiveness of antihypertensive therapy in these patient's populations. The results of these studies have shown that in patients with uncontrolled arterial hypertension, despite prolonged intake ≥ 3 antihypertensive drugs with different mechanisms of action, including a diuretic, excess sodium reabsorption persists in the distal segments of nephron due to increased aldosterone activity and sympathetic nervous system hyperactivity.

[Effect of chronic kidney disease on the formation of diastolic heart dysfunction in heart failure patients with preserved ejection fraction].

Chronic kidney disease is observed in most patients with CHF with preserved ejection fraction (HFpEF) and presents a major risk factor facilitating development and progression of LV diastolic dysfunction. The review focused on the effect of chronic kidney disease on intracellular signaling pathways affecting stiffness and diastolic relaxation of cardiomyocytes in response to inflammation and endothelial dysfunction of coronary capillaries, excessive sympathetic activation, and dysregulation of natriuretic peptides, which directly participate in the development of CHF. Elucidation of these mechanisms allows to identify new cell targets for new approaches to drug therapy for patients with HFpEF.

[INTERACTION OF BETA-BLOCKER PROPRANOLOL WITH RENIN-ANGIOTENSIN SYSTEM INHIBITORS IN RAT KIDNEY].

Propranolol injection (0.5 mg/kg, s.c.

[Interaction of renin-angiotensin system inhibitors with dopamine in rat kidney].

Dopamine (1 mg/kg, s.c.) causes 2.

[Effect of the third generation beta-blockers on ion-regulating renal function in rats with heart failure model].

Beta-adrenoceptor blockers nebivolol and carvedilol do not affect diuresis and renal sodium excretion in intact rats, but significantly increase urinary excretion of sodium in animals with a model of heart failure caused by excessive physical exercise and injection of phenylephrine. Nebivolol, in contrast to carvedilol, causes additional increase the urinary potassium loss, which is retained in animals with experimental heart failure. It is concluded that both drugs increase renal sodium excretion in rats with heart failure model by preventing the excessive sodium delay in the body.