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At least 1,351 records · Page 75Linked to original sources
PubMed2003

Biological activities of synthetic saponins and cardiac glycosides.

Comparisons of the biological activities of diosgenyl (DIO) beta-D-xylopyranosyl- (1 --> 2)-alpha-D-glucopyranoside (2DXalpha) and beta-D-glucopyranosyl- (1 --> 3)-beta-D-glucopyranoside (3GLbeta) or methyl glycyrrhetinate (GAM) 2DXalpha and 3GLbeta with those of the other DIO- or GAM- glycosides confirmed our assumption that both haemolytic and antifungal activities of DIO-glycosides (steroid saponins) generally parallel each other, while almost all haemolytic GAM-glycosides (triterpenoid saponins) have no antifungal activity. By comparisons of digitoxigenyl (DIG) 2DXalpha, beta-D-xylopyranosyl- (1 --> 2)-beta-D-glucopyranoside (2DXbeta) and 3GLbeta with the other DIG-glycosides, the previous supposition on DIG-diglycosides (cardiac diglycosides) has been developed into the assumption that those having a (1 --> 4), (1 --> 3) or (1 --> 2)beta sugar linkage show stronger anti-ATPase and antiviral activities than those with a (1 --> 6) or (1 --> 2)alpha linkage.

Adenosine Triphosphatases↗
PubMed1985

Cardiac glycosides, calcium and the release of neurotransmitter from peripheral noradrenergic nerves.

The requirement for external Ca (Cao) of neurotransmitter release evoked by cardenolides has been investigated in canine saphenous vein. Basal efflux of 3H-compounds from saphenous veins pre-loaded with 3H-noradrenaline was the same in the absence as in the presence of Cao; Cao is not required for basal efflux of neurotransmitter. Efflux of 3H-compounds was increased by cardenolides. Both ACS and ouabain caused a similar maximum net efflux of 3H suggesting that each evokes release from the same pool of 3H compounds. The similarity of the effects obtained with cardenolides to those obtained during exposure of saphenous vein preparations to potassium-free media suggests that 3H-efflux is the result of Na,K-ATPase inhibition. With ACS (ca. EC50) the net efflux of 3H-compounds early (less than 60 min) in the release period was greater in the absence of Cao than in its presence whereas at longer times the reverse was true; net efflux was less in the absence of Cao than in its presence. The difference in the 3H-efflux pattern was paralleled qualitatively throughout by efflux of 3H-noradrenaline. The ACS-evoked efflux of 3H-compounds in the presence and absence of Cao derives from sympathetic, noradrenergic nerves; 3H present in extraneuronal tissues was not released by the cardenolide. With ouabain (less than EC50) the total efflux of 3H over a 75 min period was greater in the absence of Cao than in its presence. The reverse was found with ouabain (greater than EC50): the total efflux of 3H was less in the absence of Cao than in its presence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Accumulation of radioactive cardiac glycosides by various brain regions in relation to the dysrhythmogenic effect.

Ouabain was administered at a loading dose of 3 mug/kg followed by an infusion at a rate of 1 mug/kg-1 min-1 in order to produce severe dysrhythmia in dogs within 60 minutes. Similarly, digitoxin at a loading dose of 9 mug/kg followed by an infusion at a rate of 3 mug kg-1 min-1 was administered to compare its effect with that of ouabain. 2 During the 60 min experimental period, the plasma concentrations gradually rose with the continuous infusion of these drugs. However, in comparison to the 60 min plasma value of 119+/-20 pmol/ml for ouabain and 177+/-68 pmol/ml for digitoxin, the cerebrospinal fluid (CSF) concentrations for these drugs at this time were less than 5 pmol/ml. 3 Upon termination of the experiment at 60 min it was found that kidney, liver, heart, adrenal, and the non-neural tissue in the brain such as pituitary and choroid plexus concentrated ouabain and digitoxin to give high tissue to plasma ratios. However, various neural areas of the brain (cerebellum, mesencephalon, hypothalamus, pons, and medulla) showed no preferential localization or uptake of these two glycosides. 4 Concentration of ouabain and digitoxin by the choroid plexus does not seem to affect the ionic composition of the CSF. 5 It was concluded that sampling the large areas of neural tissue above could provide no evidence for local accumulation of digitalis glycosides that might account for a central nervous system origin of digitalis-induced cardiac arrhythmias.

Animals↗
PubMed1984

Haemodynamic effects of prenaterol and cardiac glycosides in patients with recent myocardial infarction.

Prenalterol was given to twenty five patients with acute myocardial infarction. Thirteen patients (group B) had signs of cardiac decompensation while twelve (group A) had not. Ejection fraction was determined with 99mTc-labelled red blood cells before and after prenalterol (50 micrograms kg-1 body weight), intravenously. In group B this procedure was repeated after digitalization 2 days later. The ejection fraction increased significantly in group A after prenalterol injection. In group B, prenalterol produced an increase, but this was not significant. After digitalis the ejection fraction increased significantly and prenalterol produced an additional significant rise. No significant changes in blood pressure occurred. Heart rate increased significantly in both groups after prenalterol injection and decreased significantly after digitalis.

Adrenergic beta-Agonists↗
PubMed1989

Modification of the positive inotropic effects of catecholamines, cardiac glycosides and Ca2+ by the orally active male contraceptive, gossypol, in isolated guinea-pig heart.

Gossypol is an orally active male contraceptive with cardio-depressant side effects. To understand the mechanism of its cardiac actions, the interaction of gossypol with positive inotropic drugs was examined in isolated atrial muscle preparations obtained from guinea-pig heart. Gossypol delayed the onset of arrhythmias caused by digoxin. In the presence of gossypol, the positive inotropic effect of isoproterenol declined rapidly, and the effect of isoproterenol to increase tissue cyclic AMP concentrations was smaller. Pretreatment of atrial muscle with the combination of gossypol and isoproterenol markedly reduced effects of isoproterenol on developed tension and cyclic AMP concentrations when these effects were tested after the washout of the first dose of isoproterenol. These effects, however, were not specific to isoproterenol. The gossypol-isoproterenol pretreatment reduced the positive inotropic effect of ouabain or extracellular Ca2+. These results indicate that gossypol has pharmacodynamic interactions with several positive inotropic agents that are known to enhance developed tension by increasing intracellular Ca2+ transients.

Animals↗
PubMed1984

Cardiac glycoside receptors in cultured heart cells--II. Characterization of a high affinity and a low affinity binding site in heart muscle cells from neonatal rats.

The binding of [3H]ouabain has been studied in (Na+ + K+)-ATPase enriched cardiac cell membranes, as well as in cardiac muscle and non-muscle cells in culture--all obtained from hearts of neonatal rats. The binding has been correlated with ouabain-induced inhibition of (Na+ + K+)-ATPase (cardiac cell membranes) and the inhibition of active (86Rb+ + K+)-influx (cardiac muscle and non-muscle cells in culture). Furthermore, the effect of ouabain on the amplitude of cell-wall motion and contraction velocity has been studied in electrically driven cardiac muscle cells. In muscle and non-muscle cells, two classes of ouabain binding sites have been identified. In rat heart muscle cells, the high affinity binding site has a dissociation constant (KD) of 3.2 X 10(-8) M and a binding capacity (B) of 0.2 pmole/mg protein (80,000 sites/cell); the values for the low affinity binding site are: KD = 7.1 X 10(-6) M; B = 2.6 pmole/mg protein (10(6) sites/cell). The binding to both types of binding sites is depressed by K+ and abolished after heat denaturation of the cells. The kinetics of [3H]ouabain binding to rat heart muscle cells (association and dissociation rate constants, K+- and temperature-dependence of association and dissociation processes) have been characterized. In rat heart muscle and non-muscle cells, the binding of [3H]ouabain to the low affinity site results in inhibition of the (86Rb+ + K+)-influx (EC50 = 1.3 and 1.5 X 10(-5) M ouabain), a decrease in cell-K+ (EC50 = 1.9 and 1.4 X 10(-5) M) and an increase in cell-Na+ (10(-5)-10(-4) M). The ouabain-induced positive inotropic effect (increase in amplitude of cell-wall motion, increase in contraction velocity) in cardiac muscle cells is observed only at ouabain concentrations greater than or equal to 5 X 10(-6) M, and it is therefore probably attributed to occupation of the low affinity binding site. Coupling of occupation of the low affinity site by ouabain with drug-induced inhibition of the sodium pump and with drug-induced positive inotropic action is further substantiated by kinetic measurements. In contrast, occupation of the high affinity binding site does not produce any measurable inhibition of the sodium pump activity or positive inotropy.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Effect of transient vagal cold blockade upon reflex actions of a polar and nonpolar cardiac glycoside.

To determine the role of vagal afferent fibers in expressing the actions of a polar aminosugar digitalis agent [ASI-222 (4-amino-galactose beta-D-digitoxigenin HCl)] and a nonpolar neutral sugar agent (digoxin) on cardiac sympathetic nerve activity (CSNA), we utilized a period of vagal cooling to block traffic in that nerve. Anesthetized dogs were prepared to measure CSNA in efferent fibers from the right stellate ganglion. Both vagi were exposed midcervically and fitted with water-filled glass coils. The vagi were cooled (approximately 4 degrees C) and then either ASI-222 or digoxin was infused i.v. at dose rates which produce cardiac arrhythmias after about 100 min. Saline was infused in a third group. After 50 min of drug infusion, the vagi were rewarmed. During vagal cooling and infusion of saline or ASI-222, CSNA rose by 25 to 30%. Within 10 min after rewarming, CSNA returned to base line values in the saline group but nerve activity in the ASI-222 group promptly fell about 45% below base line and remained depressed. This dose rate of ASI-222 depresses CSNA in neurally intact dogs within 30 min. In contrast, during vagal cooling digoxin caused a slow but progressive fall in CSNA (approximately 20%); with rewarming and higher doses, CSNA began to rise above base-line levels. This profile of changes in CSNA to digoxin is similar to that observed in neurally intact animals. In other dogs given atropine to block the effects of efferent vagal nerve traffic, ASI-222 produced a prompt decline in CSNA like that observed previously in neurally intact dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗