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The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
This is a list of adrenergic drugs. These are pharmaceutical drugs , naturally occurring compounds and other chemicals that influence the function of the neurotransmitter epinephrine (adrenaline). Receptor ligands
In accordance with this, drugs that affect 5-HT-containing cells or 5-HT receptors are effective treatments for numerous indications, including depression, anxiety, obesity, nausea, and migraine. Because serotonin and the related hormone melatonin are involved in promoting sleep, they counterbalance the wake-promoting action of increased ...
Beta 3 receptor is a G-protein coupled receptor, similar to beta-1 and beta-2 receptors. [7] The receptor is involved in G-as activation. [7] The receptor will also stimulate adenylyl cyclase. [7] Eventually, it will lead to effects like increase of tryptophan and 5-hydroxytryptamine level, increase of lipolysis in adipose tissue. [7]
SSRIs inhibit the reuptake of serotonin. As a result, the serotonin stays in the synaptic gap longer than it normally would, and may repeatedly stimulate the receptors of the recipient cell. In the short run, this leads to an increase in signaling across synapses in which serotonin serves as the primary neurotransmitter.
A parasympathomimetic drug, sometimes called a cholinomimetic drug [1] or cholinergic receptor stimulating agent, [2] is a substance that stimulates the parasympathetic nervous system (PSNS). [ 3 ] [ 2 ] These chemicals are also called cholinergic drugs because acetylcholine (ACh) is the neurotransmitter used by the PSNS.
Diagram of nicotinic receptor (Acetylcholine receptor) The main difference between the two major classes of neuromuscular blocking agents is their respective reversal process of paralyzing effects. Non-depolarizing blockers are reversed through acetylcholinesterase inhibitor drugs which increase the concentration of acetylcholine. [1]
Higher selectivity is associated with less off-target binding, which is binding between drug molecules and receptors other than target receptors. [6] Therefore, non-selective adrenergic blockers can cause various adverse effects as they can also exert actions on non-target receptors, such as non-selective alpha blockers and beta blockers.