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Biomedical subjects

N V Krishtal'

Publications and source records attributed to N V Krishtal'.

11 recordsLinked to original sources
PubMed1993

[The mechanisms of disorders of carbohydrate metabolism in changes to the acid-base balance].

Experiments on white rats found that both chronic acidosis and chronic alkalosis cause fasting hyperglycemia and decreases glucose tolerance. In hypophysectomized animals, alkalosis causes similar effects and acidosis leads to hypoglycemia. Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. Glucagon levels remain increased in chronic alkalosis. It has been concluded that primary cause of diabetogenic action of chronic acidosis is glucocorticoid hyperfunction and exhausting stimulation of B cells with glucose. Alkalosis causes a direct inhibitory action on B cells and activates A cells of Langerhans' islets.

Acid-Base Imbalance↗
PubMedDate not supplied

[Effect of prostaglandin E2 on ion regulating and acid excretory function of the kidneys].

Prostaglandin E2 action on ion regulating and acid excretory function of the kidneys was investigated in acute experiments on intact male rats whose angiotensin-converting enzyme (ACE) had been blocked by enalapril. It was shown that i.p. two-fold PGE2 injection (0.5 mg/kg) during water load decreased diuresis, glomerular filtration, excretion of potassium, titration acids, ammonium, and increased urine pH. Sodium excretion was detected only if ACE had been blocked. In both series of experiments, an increase in chloride excretion was found to be statistically significant. A conclusion has been made that PGE2 influences directly the inhibition of acid excretory function of the kidneys.

Acids↗
PubMedDate not supplied

[The adrenergic and dopaminergic regulation of kidney acid-excreting function].

It has been found in experiments on white rats that the activation of peripheral alpha 1-adrenoreceptors and dopamine receptors of type I stimulates acid-excretory renal function with inhibition of the angiotensin-aldosterone system. The blockade of alpha 1-adreno- and dopamine receptors depresses acid-excretory renal activity. The activation and inhibition of beta-adrenoreceptors do not change the excretion of hydrogen ions. The role of the activation of peripheral alpha 1-adreno- and dopamine receptors in compensatory reactions of the organism at metabolic acidosis is discussed.

Animals↗
PubMedDate not supplied

[Adrenergic effects on the renal function and their mechanisms].

The experiments on rats have shown that the activation of alpha-adrenoceptors decreases the glomerular filtration as well as sodium and water reabsorption against a background of a decrease in the blood content of vasopressin, renin, angiotensin II, aldosterone and a fall of the renal cortex level of thromboxane B2. alpha-, alpha 1- and beta-adrenoceptors blockade decreases diuresis as well as sodium and potassium excretion due to an increase in the level of vasopressin, renin and insulin. The stimulation of beta-adrenoceptors accelerates the glomerular filtration, decreases sodium reabsorption and potassium excretion against a background of an increase in the secretion of vasopressin, renin, insulin and a fall of the blood level of angiotensin II and aldosterone and an elevation of the prostaglandin E2 content in the renal cortex. A conclusion is drawn that the adrenergic regulation of the kidneys is mediated to a considerable degree by hormones which regulate the water-salt metabolism and vascular tonus in vivo.

Animals↗
PubMedDate not supplied

[Role of the hypophyseo-adrenal system in regulating the acid-secreting function of the kidneys].

The experiments on male albino rats have shown that both stress and hydrocortisone elevate the urinary excretion of hydrogen ions in the form of titrated acids and ammonium ions. Desoxycorticosterone acetate (DOCSA) in intact rats, adrenal- and hypophysectomy lower ammonium ions excretion. Both stress and DOCSA increase the tubular sodium reabsorption, while hydrocortisone, adrenal- and hypophysectomy decrease it. A conclusion is made that both glucocorticoids and mineralocorticoids participate in the renal functional change under stress. It should be underlined that glucocorticoids stimulate the secretion while mineralocorticoids play the leading part in maintenance of sodium homeostasis.

Acids↗
PubMedDate not supplied

[Mechanisms of renal adaptation to disorders of water-electrolyte balance in metabolic acidosis].

The albino rat experiments have demonstrated that despite the type, metabolic acidosis causes an increase in plasma and urinary osmolarity, hyperkalemia and hypernatremia, enhanced urinary excretion of potassium, phosphates, and titrated acids with a tendency for the glomerular filtration rate and urinary pH to be lowered with the increased concentrations of plasma vasopressin and insulin and renal cortical PGE2. Hyperchlorinemic acidosis without increases in the anion difference is accompanied by severe chloremia, natriuresis, chloruresis, ammoniuresis without diuretic changes with the inhibited renin-aldosterone system and progesterone synthesis. Lactate acidosis with a growing anion difference leads to lower diuresis, Na+ and Cl- excretion without enhancing ammonium excretion in the presence of elevated plasma levels of renin, aldosterone, and progesterone. It is concluded that in metabolic acidosis, adaptation to water-electrolytic exchange derangements greatly depends upon the type of metabolic acidosis and it is mediated by hormones to a considerable extent.

Acidosis↗
PubMedDate not supplied

[Endocrine regulation of chlorine ion transport in rat kidneys].

Eighty-five intact, adrenalectomized and hypophysectomized white male rats fed low-caloric diets were used in experiments. Hormonal effects on urinary excretion of chlorides and sodium were studied in hyperhydration conditions; these hormones' levels are elevated in metabolic acidosis. Experiments have demonstrated that corticotropin in intact animals and hydrocortisone in hypophysectomized ones increased chlorine ions elimination without increasing sodium withdrawal. On the contrary, adrenal- and hypophysectomy reduced Cl- excretion without changing Na+ excretion. Vasopressin and insulin increased Na+ excretion and, to a much greater measure, Cl- excretion. The author comes to a conclusion that urinary excretion of chlorine ions not bound to sodium, conducive to accumulation in the blood of bicarbonate, is regulated in metabolic acidosis by corticotropin, glucocorticoids, vasopressin, and insulin.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[The participation of the renin-angiotensin-aldosterone system in the pathogenesis of acute kidney failure in endotoxemia].

It was found in acute experiments on white rats that injection of Salmonella typhimurium lipopolysaccharide activates renin-angiotensin-aldosterone system (RAAS) and causes oligohydruria form of acute renal failure (ARF). Enalapril, angiotensin-converting enzyme, being injected simultaneously with endotoxin, increases diuresis, glomerular filtration rate, electrolytes excretion and reabsorption by proximal tubules, decreases proteinuria and blood nitrogen-down to the normal. Thus, RAAS takes part in endotoxemia ARF induction and enalapril has protective effect.

Acute Kidney Injury↗