Strophanthidin was used to synthesize acetylstrophanthidin and the effect on neurotransmitter release from dog saphenous vein was studied.3
Biochem/physiol Actions
Strophanthidin is a cardiotonic steroid that elevates the activity of Na+/K+-ATPase in cardiac myocytes.1 It decreases the potassium content and raises the sodium content in rabbit renal cortex slices.2
Three horses died as a result of eating grass hay containing summer pheasant's eye (Adonis aestivalis L.), a plant containing cardenolides similar to oleander and foxglove. A 9-year-old thoroughbred gelding, a 20-year-old appaloosa gelding, and a 5-year-old quarter horse gelding
Tissue damage at the time of organ transplantation has a negative impact on the subsequent success of the procedure, both in the immediate and longer term. Hypothermia is the principal element used to prolong organ viability ex vivo, but paradoxically
Journal of neurophysiology, 96(1), 109-118 (2006-02-10)
Cell-attached and whole cell recording techniques were used to study the effects of electrogenic sodium pump on the excitability of rat suprachiasmatic nucleus (SCN) neurons. Blocking the sodium pump with the cardiac steroid strophanthidin or zero K+ increased the spontaneous
The Journal of physiology, 575(Pt 3), 845-854 (2006-07-11)
Glycoside-induced cardiac inotropy has traditionally been attributed to direct Na(+)-K(+)-ATPase inhibition, causing increased intracellular [Na(+)] and consequent Ca(2+) gain via the Na(+)-Ca(2+) exchanger (NCX). However, recent studies suggested alternative mechanisms of glycoside-induced inotropy: (1) direct activation of sarcoplasmic reticulum Ca(2+)
Journal of neurophysiology, 90(5), 3119-3129 (2003-08-02)
Disinhibition-induced bursting activity in cultures of fetal rat spinal cord is mainly controlled by intrinsic spiking with subsequent recurrent excitation of the network through glutamate synaptic transmission, and by autoregulation of neuronal excitability. Here we investigated the contribution of the
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