Pathways

Tocainide is an orally active class 1b antiarrhythmic agent that interferes with cardiac sodium channels and typically used to treat ventricular arrhythmias. It is used to treat conditions including sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. Tocainide acts in neurons where it inhibits voltage gated sodium channels in the pre synaptic neurons. In neurons, voltage gated sodium channels allow sodium to come into the neuron triggering the depolarization phase. the potassium channels are responsible for the repolarization phase to bring the neuron back to resting potential. The action potentials created travel down the axon of the neuron and at the nerve terminal, calcium channels open, allowing calcium to enter the cell. Calcium entry causes synaptic vesicles containing neurotransmitters like glutamate to fuse with the membrane and expel the neurotransmitter into the synapse. Glutamate binds to AMPA and NMDA receptor on the post synaptic neurons where they cause excitation of the neuron. By blocking the voltage gated sodium channels, carbamazepine prevents the depolarization phase, inhibiting action potential generation and the release of excitatory neurotransmitter like glutamate. Pre and post synaptic neuronal firing are therefore reduced. Tocainide works as a “use-dependent” block. This means that it preferentially binds to channels that are being opened. In neurons that are repetitively firing, their sodium channels are being opened more often, and as a result, tocainide is able to produce a greater block in these neurons. It also possesses some anticholinergic and local anesthetic properties. Side effects of tocainide include nausea, vomiting, headaches, feeling dizzy, or feeling hot and flushed.

Tocainide is an orally active class 1b antiarrhythmic agent that interferes with cardiac sodium channels and typically used to treat ventricular arrhythmias. It is used to treat conditions including sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. Tocainide is a primary amine analog of lidocaine with antiarrhythmic properties useful in the treatment of ventricular arrhythmias. Tocainide, like lidocaine, produces dose dependent decreases in sodium and potassium conductance, thereby decreasing the excitability of myocardial cells. In experimental animal models, the dose-related depression of sodium current is more pronounced in ischemic tissue than in normal tissue. Tocainide is a Class I antiarrhythmic compound with electrophysiologic properties in man similar to those of lidocaine, but dissimilar from quinidine, procainamide, and disopyramide.Tocainide binds preferentially to the inactive state of the sodium channels. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. It also possesses some anticholinergic and local anesthetic properties. Side effects of tocainide include nausea, vomiting, headaches, feeling dizzy, or feeling hot and flushed.

Metabolites of Tofacitinib are predicted with biotransformer.

Tolazamide is an hypoglycemic agent from the sulfonylurea class used in the treatment of non insulin dependent diabetes mellitus type II. Tolazamide lowers blood glucose by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. This drug binds to ATP-sensitive potassium-channel receptors on the pancreatic cell surface (known as the sulfonylurea receptor 1 (SUR1) subunit (Kir6.2)), reducing potassium conductance and causing depolarization of the membrane. This depolarization stimulates the calcium ion influx through voltage-sensitive calcium channels thus raising intracellular concentrations of calcium ions. The higher concentration of intracellular calcium ions induces the secretion (exocytosis) of insulin into the blood. Tolazamide is administered as an oral tablet.

Metabolites of Tolazamide are predicted with biotransformer.

Tolazoline is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Tolazoline passes through the liver and is then excreted from the body mainly through the kidney.