Electrolytes In Rats Research Articles

Effects of naringenin and silymarin on urinary excretion of water and electrolytes in rats

AbstractThe effects of two flavonoid derivatives, naringenin and silymarin on urinary excretion of water and electrolytes were investigated in isotonic saline loaded rats. Both compounds, especially naringenin, showed a moderate diuretic activity, in comparison with furosemide, increasing significantly the renal loss of sodium, chloride and potassium. With respect to silymarin, although urinary excretion was significantly lower, it caused a marked decrease in potassium excretion. These results indicate that naringenin has a diuretic behaviour similar to moderate‐efficiency diuretic agents and silymarin to potassium‐sparing diuretics.

Effects of steroids and cyclosporin a on compensatory renal growth and plasma electrolytes in rats

The uninephrectomized rat presents a reasonable model for the kidney transplant patient and allows for the study of the actions of steroids and immunosuppressive agents under conditions of stimulated renal growth. Following 2 weeks of treatment, neither cyclosporin A nor corticosterone affected the growth of the remaining kidney. The degree of compensatory renal hypertrophy was inhibited to some extent by the administration of prednisone. Renal concentrations of protein and nucleic acids were relatively uninfluenced by these agents, compared with uninephrectomized control values. Testosterone caused little change in renal mass but did incur significant reductions in protein and RNA levels, suggestive of a protein catabolic action. In examining the plasma levels of electrolytes normally handled by the kidney, testosterone also gave rise to losses of plasma potassium and calcium, whereas cyclosporin A administration led to a more pronounced lowering of calcium and magnesium levels. More detailed studies of the actions of these drugs on renal growth and function are desirable in view of their clinical potential and usage.

The effects of long-standing hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats

Experiments were performed to assess the effect of long-standing (4–8 weeks) left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. In this study the hypertension (and therefore the hypertrophy) was of long (4–8 weeks) duration. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to a respiratory acidosis (by varying the concentration of inspired PCO 2). As described previously [Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131–141], in the earlier stages of left ventricular hypertrophy (1–4 weeks duration) left ventricular pHi was significantly alkaline at normal levels of extracellular pH. At this later stage, with the exception of animals with aortic constriction, pHi had returned to control values. There was no change in resting levels of pHi in right ventricular or skeletal muscle tissue in any hypertensive group. The improved control of pHi in left ventricular tissue observed with hypertrophy of short duration (1–4 weeks [Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131–141]) persisted in all experimental groups at this stage (4–8 weeks) after the onset of development of left ventricular hypertrophy. There was no change in pHi control in right ventricular or skeletal muscle tissue. Neither was there any change in intracellular electrolyte concentrations or content in association with hypertension in any tissue or group studied.

The effects of short-term hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats

Experiments were performed to assess the effect of left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either: (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to an acute respiratory acidosis (by varying the concentration of inspired PCO 2). In association with left ventricular hypertrophy (secondary to hypertension), left ventricular pHi became significantly alkaline in all experimental hypertensive groups compared with control values; pHi control (in response to an acidosis) was also significantly improved. There was no change in resting levels of pHi or pHi control in right ventricular or skeletal muscle tissue in any hypertensive group. There was no change in resting levels of pHi or pHi control in left ventricular, right ventricular or skeletal muscle tissue from sham-operated animals. This suggests that these changes are the result of hypertrophy per se, rather than due to a generalised mechanism secondary to hypertension and operating on all tissues. There was no change in intracellular electrolyte concentration or content in association with hypertension in any tissue or group studied.

O-31 - Effects of bunazosin on blood pressure, sympathetic nerve activity, urinary catecholamines and urinary electrolytes in rats

O-31 - Effects of bunazosin on blood pressure, sympathetic nerve activity, urinary catecholamines and urinary electrolytes in rats

Effects of atrial natriuretic factor on renal handling of water and electrolytes in rats.

The intravenous injection of an extract of atrial myocardium into anesthetized rats during a hypotonic diuresis resulted in an increase in the renal excretion of water, sodium, potassium, calcium, magnesium, and phosphate. There was an increase in urine concentration which was probably a result of the secretion of vasopressin since it did not occur in Brattleboro (di/di) rats. A transient increase in glomerular filtration rate and renal plasma flow occurred during the first five minutes with a more sustained rise in filtration fraction. Injection of atrial extract also caused a partial inhibition of solute-free water formation in Brattleboro rats subjected to water diuresis and a partial inhibition of solute-free water reabsorption in rats subjected to maximal antidiuresis by infusing vasopressin. In neither case was the degree of inhibition as profound as that observed after injecting furosemide in a dose which caused a comparable natriuretic response. A large dose of furosemide blocked the natriuretic response to atrial extracts whereas, when a comparable level of sodium and water output was produced by massive infusions of saline, the natriuretic response to atrial extract was increased. It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Furosemide might also act at the same tubular site or inhibit tubular secretion of the atrial natriuretic factor.

Pharmacological studies of 2-(5H-[1]benzopyrano[2,3-b]pyridin-7-yl) propionic acid (Y-8004) (II). General pharmacological action

This anti-inflammatory agent proved to have a therapeutic margin wider than that of indomethacin. Y-8004 exhibited little effect on the central nervous system, somatic and autonomic nervous system. On the cardiovascular system in dogs, Y-8004 induced a slight transient fall in blood pressure followed by a pressor response, increase in heart rate and coronary vasodilation at a dose of 30 mg/kg given intravenously, but no remarkable change was seen on the electrocardiogram. Y-8004 showed no effect on isolated smooth muscles such as vas deferens, ileum and atria, but inhibited gastrointestinal propulsion at a dose of 100 mg/kg given orally in mice and spontaneous contractions of the pregnant uterus of rats at a concentration of more than 10(-6)M. This agent also decreased urine volume and electrolytes in rats. This property was considered to be common to other acidic nonsteroidal anti-inflammatory agents. On the other hand, in guinea pigs, Y-8004 inhibited the bradykinin-induced bronchoconstriction and the collagen-induced platelet aggregation to a greater extent than did indomethacin. These findings suggest that Y-8004 is an active compound with properties similar to acidic non-steroidal anti-inflammatory agents such as indomethacin.

Pharmacological studies on bamboo grass. (2) Central depressant and antitoxic actions of a water-soluble fraction (folin) extracted from Sasa albomarginata Makino et Shibata

Folin administered showed a significant antagonistic effect to caffeine induced hyperactivity and slightly prolonged hexobarbital induced sleeping time in mice. An antitussive effect was evident only with high doses and anticonvulsant effects were not observed. A mixture of Folin with HgCl2, NaAsO2, 3CdSO4-8H2O or tetrodotoxin resulted in an apparent decrease in mortality rates. However Folin had no effect in the case of alternate administration with a poison or preadministration of Folin. As other pharmacological properties of Folin, a protective effect on induced stress ulcer in rats and an increase in acid output in pylorus-ligated rats in which aspirin was administered. Folin had no inhibitory effect on reserpine ulcer and acetic acid induced anal ulcer in the rat. Neither an increase in gastric motility nor cathartic effect was observed with Folin. In addition, Folin showed a tendency of inhibition on heat induced edema and increase of urinary vikyne and electrolytes in rats.

Changes in Muscle and Brain Electrolytes in Rats Fed Natural Imbalanced Diets

Changes in Muscle and Brain Electrolytes in Rats Fed Natural Imbalanced Diets

Effects of diuretic agents on serum and tissue electrolytes in rats.

Summary and ConclusionsHydrochloro thiazide, polythiazide and chlorthalidone were added to the diets of 3 groups of Sprague-Dawley rats. After 4 weeks of subsistence on this diet, these animals together with matched controls were sacrificed and analyses of serum and tissue electrolytes were done. The serum chloride concentration was significantly lower in each experimental group. Serum potassium concentration was decreased in all 3 groups, and was significantly lowered in the groups receiving chlorthalidone and hydrochlorthiazide. Changes in serum sodium concentration were not statistically significant. Tissue analyses revealed no significant alterations in water or electrolyte content. These studies suggest that the hypokalemia associated with oral diuretic therapy results from a redistribution of potassium stores rather than a frank depletion of this ion in rats.

Effect of salicylate on plasma magnesium-levels.

IN this laboratory a recent examination of the distribution of electrolytes in rats following the repeated administration of both sodium and potassium salicylate has shown that a marked decrease in the excretion of urinary magnesium occurs. Evidence of a less well-defined increase in the level of plasma magnesium was also found1.

Kidney electrolyte in rats with alkalosis associated with potassium deficiency.

Kidney electrolyte in rats with alkalosis associated with potassium deficiency.

Muscle electrolytes in rats following ischemia produced by tourniquets.

Muscle electrolytes in rats following ischemia produced by tourniquets.