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

Dopamine (1 mg/kg, s.c.) causes 2.2-fold increase in diuresis (p < 0.05) in anesthetized rats, which is accompanied by an increase in the urinary excretion of sodium and potassium by a factor of 2.2 and 2.8, respectively (p < 0.05). Preliminary administration of the ACE inhibitor enalapril (1 mg/kg, p.o., for 7 days) enhances the renal dopamine response with 3.5-fold increase in its diuretic effect and increases natriuresis 3.2 times and urine potassium excretion 5 times (p < 0.05). After preliminary introduction of the AT1-angiotensin receptor antagonist losartan (1 mg/kg, p.o., for 7 days) dopamine causes 3.3-fold increase in diuresis, 3.1-fold increase in natriuresis, and 3-fold increase in kaliuresis (p < 0.05). Preliminary administration of the direct renin inhibitor aliskiren (4 mg/kg, p.o., for 7 days) is accompanied by 6-fold increase in the diuretic effect of dopamine and increases natriuresis 7.2 times and urine potassium excretion 7 times (p < 0.05). It is concluded that renin-angiotensin system (RAS) of renal tissues is involved in the mechanism of dopamine action in the kidney, acting as a modulator that prevents excessive loss of water and electrolytes with urine.

[Nephroprotective properties of third-generation beta-adrenoblockers].

Experimental and clinical data on the nephroprotector properties of third-generation beta-adrenoblockers nebivolol and carvedilol are reviewed. These properties are related to the antihypertensive effect and ability of drugs to suppress oxidative stress in glomerules, proximal renal tubules, and surrounding interstitial tissue.

[Analysis of the role of neurohumoral systems in action of dopaminomimetic dopamine on ion-regulating renal function].

Dopamine causes in anesthetized rats expressed diuretic response that is accompanied by an increase in GRF and a significant enhance of sodium and potassium excretion. Pretreatment the animals in diclofenac sodium or contrical in doses, that inhibit respectively activity of renal PG-system and kallikrein-kinin system, don't prevent of renal effects of dopamine. Preliminary assignment a direct renin inhibitor aliskiren enhances the diuretic, natriuretic and kaliyuretic effects of the drug. It is concluded that renal PG-system and kallikrein-kinin system are not involved in the formation of renal effects of dopamine. Renal tissue RAS directly included in the mechanism of action of dopamine in the kidney, acting as a modulator, preventing excessive loss of water and electrolytes with urine.

[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.

[The interaction of the converting-enzyme inhibitor captopril with cardiac glycosides in the rat kidney]. / Vzaimodeistvie ingibitora konvertiruiushchego fermenta kaptoprila s serdechnymi glikozidami v pochke krysy.

Strophanthin (0.1 mg.kg, i.v.) and digoxin (0.1 mg/kg, i.v.) moderately increase blood supply of the renal cortical and medullary layers in unconscious rats and enhance renal excretion of sodium and water. Preadministration of the converting enzyme inhibitor captopril (10 mg/kg/day, per os, for 6 days) promoted vascular dilatation in the inner and outer areas of the medulla, which occurred under the action of these agents and substantially increased their natriuretic and diuretic effects. It is concluded that the renin-angiotension system is directly involved into the mechanism of action of cardiac glycosides in the kidneys, acting as a modulator that prevents their vasodilating and tubular effects.

[The interaction of the Ca2(+)-channel blocker verapamil with cardiac glycosides in the rat kidney]. / Vzaimodeistvie blokatora Ca2(+)-kanalov verapamila s serdechnymi glikozidami v pochke krysy.

Strophanthine (0.1 mg/kg, i. v.) and digoxin (0.1 mg/kg, i. v.) increase blood supply of the cortex and medullary layer of the kidneys of anesthetized rats and significantly raise excretion of water and sodium by the kidneys. Verapamil, a blocker of Ca(2+)-channels (0.25 mg/kg, i. v.) attenuates the increment of the blood flow in the internal zone of the cortex and external zone of the medullary layer but does not prevent the rise of diuresis and excretion of sodium with urine under the action of the above-indicated drugs. The conclusion is drawn that realization of the vasodilatory effect of cardiac glycosides in the kidneys is partially connected with a lowering of the content of Ca2+ in myofibrils whereas formation of their tubular effect does not depend on the changes in Ca2+ concentration in nephron cells.

[The influence of inhibitors of kinin biosynthesis, prostaglandins and angiotensin II on the vascular and tubular effects of strophanthin in the rat kidney]. / Vliianie ingibitorov biosinteza kininov, prostaglandinov i angiotenzina II na sosudistyi i kanal'tsevyi éffekty strofantina v pochke krysy.

Strophanthin was shown to increase the blood flow in the external, internal zones of the cortex and the external medulla of the rat kidney without influencing the blood supply to the internal zone of the medulla. Contrikal eliminates the vasodilating effect of the drug in the mentioned zones of the renal tissue and significantly increases its natriuretic action. Indomethacin also prevents the hemodynamic shift occurring in the kidneys under the influence of strophanthin but fails to change the character of the natriuretic effect of the drug. Captopril exerts no influence on the increase of the blood flow in the external medulla but eliminates the vasodilating effect of strophanthin in the cortex and significantly potentiates its natriuretic action.

[The influence of inhibitors of kinin and prostaglandin formation on the vascular and tubular effects of osmotic diuretics in the kidney]. / Vliianie ingibitorov obrazovaniia kininov i prostaglandinov na sosudistyi i kanal'tsevyi éffekty osmoticheskikh diuretikov v pochke.

Mannit was shown to increase the blood flow in the external, middle and internal zone of the renal cortex in anesthetized rats but exerts no effect on the blood supply to the external zone of the medullary layer. A preliminary administration of contrykal fails to influence the diuretic and natriuretic effects of the preparation and to change the character of the hemodynamic shift at the action of the diuretic in the middle zone of the cortical layer. Indomethacin completely eliminates the blood flow increase in the middle zone of the cortex but it does not prevent the diuretic and natriuretic reaction to mannit administration. It is concluded that realization of the vascular and tubular effects of the diuretic is not related to the increase of kinin biosynthesis in the kidneys. Prostaglandins formed in the kidneys under the influence of mannit are involved in the mechanism of dilatation of the vessels of the cortical layer but do not play the significant role in the formation of its tubular effect.

[Effect of dopamine on the blood flow in various zones of the kidney cortex and medullary layer in rats]. / Vliianie dofamina na krotok v razlichnykh zonakh kory i mozgovogo sloia pochek krys.

Phentolamine and propranolol did not alter the kidney response to dopamine whereas haloperidol completely prevented the dopamine vascular and channel effects. The agents inhibiting cyclooxygenase and kallikrein-kinin system do not interfere with an increase in the blood flow or depressing action of the neurotransmitter upon sodium transport in the nephron. The hemodynamic shift occurring under the effect of dopamine in different areas of renal tissue seems to be due to a selective stimulation of vascular DA-receptors and unrelated to an increase in the production of prostaglandins and kinins in the kidneys.

[Effect of dopamine and its combination with furosemide on sodium transport in the rat kidney]. / Vliianie dofamina i ego kombinatsii s furosemidom na transport natriia v pochke krysy.

In experiments on rats phentolamine, propranolol, indomethacin were shown to exert no significant effect on the natriuretic action of dopamine, whereas haloperidol completely prevented it. In rats with chronic narrowing of the vena cava dopamine potentiated the diuretic and natriuretic effects of furosemide.

[Role of kidney prostaglandins, kinins and dopamine receptors in the natriuretic effect of ethacrynic acid]. / Rol' pochechnykh prostaglandinov, kininov i dofaminovykh retseptorov v natriiureticheskom éffekte étakrinovoi kisloty.

It was found in experiments on anesthetized rats that ethacrynic acid (3 mg/kg intravenously) exerted no effect on the blood flow in the internal zone of the cortical layer but significantly increased the blood supply to the median zone of this region of the kidneys. A pronounced natriuretic reaction produced by inhibition of this ion develops. An inhibitor of cyclooxygenase indomethacin (3 mg/kg orally, 5 days) completely eliminated an increase of the blood flow in the cortical median zone but failed to prevent an increase of diuresis and urinary excretion of sodium in response to the diuretic administration. An inhibitor of kallikrein contrykal (5000 U/kg subcutaneously) produced no effect on diuretic and natriuretic effects of the drug but prevented the hemodynamic shift in the renal cortex. A blocker of dopaminergic receptors haloperidol (3 mg/kg subcutaneously) caused no changes in the rat kidney response to ethacrynic acid. Prostaglandins and kinins formed in the kidneys under the influence of the diuretic are thought to be involved in the mechanism of dilatation of vessels of the cortical layer median zone but play no significant role in the formation of its natriuretic effect.

[Furosemide interaction with the prostaglandin and kallikrein-kinin systems of the kidneys]. / Vzaimodeistvie furosemida s prostaglandinovoi i kallikrein-kininovoi sistemami pochek.

Indomethacin (3 mg/kg, orally for 5 days) prevented the increase of blood flow in the internal zone of the renal cortical layer but failed to interfere with the increase of diuresis and sodium secretion produced by furosemide (2 mg/kg, subcutaneously) in anesthetized rats. Contrykal (6000 ED, subcutaneously) failed to alter the character of the hemodynamic changes in the renal cortex but enhanced the diuretic and natriuretic effects of furosemide. In unanesthetized rats indomethacin prevented creatinine urine excretion but didn't attenuate the diuretic and natriuretic effects of furosemide.

[Role of the kallikrein-kinin system and prostaglandins in the action of dopamine on blood flow and sodium transport in the rat kidney]. / Rol' kallikrein-kininovoi sistemy i prostaglandinov v deistvie dofamina na krovotok i transport natriia v pochke krysy.

In anesthetized rats, dopamine (1 mg/kg) increased the blood flow in adrenal and external medullary layers of kidneys with accompanying obvious sodium-uretic response due to inhibition of sodium reabsorption, PO2 not changing, at that. Haloperidol (1 mg/kg) prevented the hemodynamic shift and its depressing effect on the sodium transport in the kidney channels. The inhibiting agent for kallikrein-kinin system contrical and inhibiting agent for prostaglandin synthetase indomethacin did not alter the kidney response to the neurotransmitter under study. The intrarenal hemodynamic shift and inhibition of sodium transport induced with dopamine seem to be due to stimulation of renal postsynaptic dopamine receptors and unrelated to activation of the renal kallikrein-kinin system or augmentation of prostaglandins synthesis.

[Effect of a blockade of the beta 1-adrenoreceptors on the hemodynamics, oxygen tension and sodium reabsorption in the rat kidney]. / Vliianie blokady beta 1-adrenoretseptorov na gemodinamiku, napriazhenie kisloroda i reabsorbtsiiu natriia v pochke krysy.

Blockade of kidneys' beta-1 adrenoreceptors with talinolol entailed in anesthetized rats a sodium- uretic response accompanied by inhibition of sodium reabsorption and an increase of the blood flow in cortical and external layers with no PO2 changes, at that. Haloperidol prevented the increase of blood flow in the external layer but did not affect the cortical hemodynamic shift or the depressing influence of talinolol on the channel transport of sodium. The inhibiting agent for the kallikrein-kinin system contrical and the inhibiting agent for prostaglandin synthesis indomethacin did not alter the kidney response to the drug under study. The hemodynamic shift as well as the inhibition of sodium reabsorption seem to be unrelated either to excitation of receptors sensitive to dopamine, or to activation of the kallikrein-kinin system or stimulation of prostaglandin synthesis.

[Role of prostaglandin, the kallikrein-kinin system and renal dopamine receptors in the mechanism of the natriuretic action of the beta-adrenoblocker obzidan]. / Rol' prostaglandinov, kallikrein-kininovoi sistemy i dofaminovykh retseptorov pochek v mekhanizme natriiureticheskogo deistviia beta-adrenoblokatora obzidana.

It has been established in experiments on anesthetized rats that the beta-adrenoblocker obsidan inhibiting tubular sodium reabsorption in the kidneys provokes the natriuretic reaction which correlates with the increased blood flow in the cortex and in the external medullary substance. pO2 in these zones of the renal tissue remains unchanged. The inhibitor of prostaglandin biosynthesis indomethacin and the inhibitor of the kallikrein-kinin system contrykal did not affect the renal response to the drug under study. The dopamine blocker haloperidol prevented the hemodynamic shift in the cortical and in the external medullary layers and interfered with the inhibitory action of obsidan in tubular sodium transport. It is inferred that the natriuretic response to the action of beta-adrenoblockers is not linked with the increased prostaglandin biosynthesis in the kidneys or with activation of the kallikrein-kinin system but is partially governed by stimulation of dopamine receptors of the kidneys.

[Interaction of catecholamines and the renin-angiotensin system in regulating sodium reabsorption in the rat kidney]. / Vzaimodeistvie katekholaminov i sistemy renin-angiotenzin v reguliatsii reabsorbtsii natriia v pochke krysy.

It has been established that the catecholamine-induced increase in renin secretion by juxtaglomerular apparatus cells and sodium reabsorption stimulation in the rat kidney are consequent on the excitation of renal beta-adrenoreceptors. Strophanthin K interferes with the renin-secreting action of adrenaline and perverts its activating effect on sodium transport by renal tubules. When given in a dose inhibiting angiotensin II formation and renin-secreting effect of catecholamines, heparin also diminishes their activating effect on tubular sodium transport. It is suggested that the renin-angiotensin system may be directly involved into the mechanism of catecholamine-stimulated sodium reabsorption by the rat kidney.