[Effects of dopamine and adenosine on regulation of water-electrolyte exchange in Amoeba proteus].

Dopamine and adenosine both regulate transport of sodium chloride in the renal tubules in mammals. We have studied the effect of dopamine and adenosine on spontaneous activity of contractile vacuole of Amoeba proteous. Both substances stimulated contractile vacuole.

[Disease from the point of view of evolution].

In the process of evolution, such compensatory reactions as enhanced reabsorption of sodium chloride and an increase of arterial pressure could be formed only for compensation of acute pathological states (blood loss, dehydration). At present they remain similarly adequate in acute disturbances of blood circulation and of water-electrolyte balance. However, in severe chronic pathology of heart and kidney they often lose their compensatory function and even become dangerous.

[Effect of acetylcholine and acetylcholinesterase on the activity of contractile vacuole of Amoeba proteus].

Acetylcholine (ACh, 1 microM) stimulates activity of the contractile vacuole of proteus. The effect of ACh is not mimicked by its analogs which are not hydrolyzed by acetylcholinesterase (AChE), i. e.

[Effect of marinobufagenin on the primary reinforcing effect of ethanol].

Intraperitoneal administration of marinobufagenin resulted in a reliable and dose-dependent suppression of ethanol self-administration in drug- and experimentally naive DBA/2 mice. The findings suggest that Na/K-ATPase contributes to both mediation of the ethanol reinforcing properties and the mood regulation.

[The tyrosine kinase inhibitor genistein potentiates the antidiuretic effect of vasopressin and its analogs].

Genistein was shown to potentiate the effects of all the activators of the water flow except the cAMP action. The thyrosine kinase (TK) seems to suppress the hydrosmotic action of arginine vasopressin at the period preceding the cAMP formation and to potentiate this effect afterwards.

[The role of protein kinase C and muscarinic cholinoreceptors in vasopressin-stimulated water transport].

The role of protein kinase C (PKC) in the control of vasopressin-stimulated water transport in the frog urinary bladder and its modulation by M2-agonist oxotremorine has been studied. Using the PKC inhibitor, staurosporine we showed that PKC in the region pf the basal membrane suppressed vasopressin-stimulated water transport, whereas PKC in the apical region potentiated this transport. It was also found that from the two types of oxotremorine action on stimulated water transport determined by its concentration only inhibition is mediated through PKC.

[The mechanisms of the effect of furosemide on the water permeability of the frog bladder and on oxytocin-stimulated contractions of the rat uterus].

Furosemide increased the hydrosmotic water flow in the frog urinary bladder and promoted the ADH-like effect of inhibitors of phosphodiesterase cAMP, potentiated hydrosmotic effects of theophylline and serosal osmotic hypertonicity but failed to change the effect of pituitrin. Fur reversibly suppressed oxytocin-induced contractions in the rat myometrium, inhibited the activity of the frog urinary bladder PDE cAMP, whereas the activity of the enzyme from the rat medulla and myometrium was activated by saluretic. Incubation of the myometrium strips in Fur resulted in a decrease in the cAMP content of the tissue.

[Spontaneous and induced permeability of the tight junctions in the bladder epithelium of the frog Rana temporaria].

The spontaneous and induced alterations in paracellular permeability of the isolated frog urinary bladder were studied. For estimation of the tight junction (TJ) permeability, a fluorescent dye uranine was used. No morphological or functional evidences for the TJ opening were found in the autumn-winter period, both in the control and after the osmotic flow stimulation by 25 mg/ml pituitrine (P) or serosal mannitol (200 mM).

[Acetylcholinesterase and the ADH-dependent transport of water in the amphibian bladder].

It was found that acetylcholine (ACh) at the concentration of 10(-3) M inhibited ADH-stimulated water transport through the wall of amphibian urinary bladder. This effect was suggested to be caused by an interaction of ACh with acetylcholinesterase (AChE) rather than by a stimulation of the M- or N-cholinoreceptor. The inhibitory action of ACh was completely suppressed in the presence of various AChE inhibitors (physostigmine, proserine, armine, Gd-42, acridine-iodmethylate), while an inhibitor of butyrylcholinesterase (BuChE), AD-4, failed to affect it.

[Effect of oxidative metabolism inhibitors on ADH-dependent transport of water in the bladder of Rana temporaria].

It has been demonstrated that inhibitors of oxidative metabolism--rotenone, amytal, antimycin A, oligomycin and 2,4-dinitrophenol--block hydroosmotic response of the urinary bladder of the frog to pituitrin, cAMP and serosal hypertonicity caused by 200 mosm mannitol. Electron donors sodium ascorbate and phenasinemethasulphate completely abolish the inhibitory effect of rotenone and antimycin A (but not of oligomycin). It is concluded that intracellular reactions which are sensitive to the effect of the inhibitors of oxidative metabolism, begin from the step after cAMP formation.

[Concentration of water, sodium, and potassium in the tissues of rats with circulatory insufficiency caused by constriction of the thoracic portion of the inferior vena cava].

In edematous rats with circulatory insufficiency, the content of water and sodium in the muscle and liver rises while that of potassium declines per 1 g wet weight. The increased sodium and decreased potassium content in the tissues cannot be accounted for only by enlargement of the extracellular volume. In contrast to normal rats, the edematous ones show a negative linear correlation between the content of sodium and potassium in the muscle and liver.

[Kidney function and Na+-K+-ATPase and succinate dehydrogenase activity in the cells of the renal tubules of rats with constriction of the thoracic portion of the vena cava inferior].

Circulatory insufficiency in rats was induced by constriction of the thoracic portion of vena cava inferior. Two-three days after the operation renal function was studied and the activity of succinate dehydrogenase and Na+K+-ATPase in the cells of the renal tubules was determined cytochemically. On infusion of 0.

[Circulatory insufficiency and edema in experimental constriction of the thoracic segment of the vena cava inferior].

A method for reproducing circulatory insufficiency in rats by constriction of the intra thoracic portion of vena cava inferior is described. A sham operation on the control animals was restricted to thoracotomy. Rats which had been subjected to constriction of the vena cava consumed 0.

[Effect of acetylcholine on the pituitrin induced osmotic flow of water through the wall of the frog urinary bladder].

The role of intercellular pathways in the ADH-dependent water transport was studied on the frog urinary bladder by means of acetylcholine (AC) and other cholinergic compounds. AC (10(-3) M) was found to cause a strong suppression of the pituitrin-stimulated water flow. Analogous effect was produced by AC on the osmotic flow stimulated by cyclic adenosine monophosphate (cAMP) and theolin.

[Distribution of water between the extracellular and intracellular space in rats].

In anesthetized rats the renal pedicules were clamped and the solution with THO, antipyrine, thyocyanate, inulin, 22Na, 36Cl, 82Br was injected into the tail artery. The space of distribution of THO was 65.1% body weight, antipyrine--81.