Cholinergic Agonists
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
ChE is located in the nerve terminal. ACh is continually hydrolyzed and resynthesized. ACh is stored in the synaptic vesicles. After fusion of the synaptic membrane with axonal membrane, ACh gets released from synaptic vesicles by the process of exocytosis involving Ca2+ influx into the nerve terminal. After release, ACh binds with receptors on pre- or postsynaptic membrane (Rang et al., 2011). This chapter deals with the drugs, which act as cholinomimetics in the periphery at muscarinic receptors (mAChRs). Muscarinic agonists, as a group, or cholinomimetics imitate or mimic the actions of ACh. The main effects they produce resemble those of parasympathetic stimulation; hence, such drugs are also called parasympathomimetics.
Drug therapy in the cardiac catheterisation laboratory: A guide to commonly used drugs
John Edward Boland, David W. M. Muller in Interventional Cardiology and Cardiac Catheterisation, 2019
Traditionally, drugs are named according to their effect (stimulatory or inhibitory) on nerve fibres (sympathetic or parasympathetic), or according to the type of neurotransmitter or cell receptor involved (acetylcholine or norepinephrine [noradrenaline]) (see Table 23.1). Thus, Parasympathomimetic agents stimulate parasympathetic nerves; Parasympatholytic agents block or inhibit parasympathetic nerves; Sympathomimetic agents stimulate sympathetic nerves; and Sympatholytic agents block or inhibit sympathetic nerves. Cholinergic drugs stimulate receptor sites mediated by the neurotransmitter acetylcholine; and Anticholinergic drugs block acetylcholine receptors. Adrenergic drugs stimulate sympathetic neuroeffector sites for epinephrine (adrenaline) or norepinephrine (noradrenaline); and Antiadrenergic drugs block epinephrine (adrenaline) or norepinephrine (noradrenaline) receptors (note acetylcholine is not exclusively a neurotransmitter for parasympathetic sites). Most drugs are designed to mimic the activity or chemical structure of endogenous ligands and are typically classified as agonists, partial agonists, antagonists or enzyme inhibitors targeting traditional protein receptors, voltage gated ion channels, or key cellular enzymes. Table 23.1 lists the major categories of cardiac drugs according to their pharmacological modes of action. This provides a reference from which to identify and compare the individual drugs discussed herein. A common feature of cardiovascular pharmacotherapy is the notion that one class of agents is often effective for the management of multiple conditions. Important examples are medication classes such as the β-adrenoceptor antagonists and calcium channel antagonists, with drugs from both being effective treatments for hypertension, arrhythmia, angina and heart failure. The following text presents the medications in the cardiovascular pharmacology classes most relevant to the CCL.
Current and new pharmacotherapeutic approaches for glaucoma
Published in Expert Opinion on Pharmacotherapy, 2020
Wesam Shamseldin Shalaby, Vikram Shankar, Reza Razeghinejad, L. Jay Katz
Cholinergic agonists improve the outflow of aqueous humor via contraction of smooth muscles within the ciliary body and widening of the trabecular meshwork. Pilocarpine is the most widely used drug in this class, and has been shown to reduce IOP by 20–25% [12,14]. Laboratory studies of retinal neurons in rats suggest a neuroprotective effect of pilocarpine through upregulation of oxidant defense genes; however, no clinical studies support these findings in patients with glaucoma [20]. Historically, cholinergic agents were the first widely used treatments for glaucoma, but have fallen out of favor due to a myriad of local and systemic side effects [14]. Ocular side effects of parasympathomimetics include ciliary spasm, miosis, pseudomyopia, and an increased risk of retinal detachments and pupillary block. A wide array of systemic side effects such as intestinal cramps and bronchospasm have also been reported, commonly resulting in patient intolerance or medication discontinuation [14].
Brimonidine tartrate for the treatment of glaucoma
Published in Expert Opinion on Pharmacotherapy, 2019
Daniel J. Oh, Judy L. Chen, Thasarat S. Vajaranant, Mark S. Dikopf
As a consequence of alpha adrenergic activation in the iris, all generations of topical alpha agonists may alter pupil size. Earlier generations (e.g. apraclonidine) with higher alpha-1 activity led to pupillary mydriasis; however, brimonidine with high alpha-2 selectivity leads to dampening of pupillary mobility and miosis [33,34]. A number of pupillometry studies have demonstrated a moderate miotic effect of various concentrations of brimonidine, as well as an anti-mydriatic effect in scotopic conditions [35–37]. The authors believe that these effects may provide utility in primary angle closure (PAC) and pigmentary dispersion syndrome (PDS). In PAC, contact between the iris and crystalline lens leads to resistance of aqueous outflow from the posterior chamber, anteriorly bowing peripheral iris into the trabecular meshwork (TM). Laser or surgical treatments to relieve this iridolenticular contact are essential, as early relief of contact may prevent irreversible TM damage. When adjunctive medical therapy is employed, brimonidine may be preferable, as the induced miosis may pull peripheral iris from contacting the TM. While parasympathomimetic agents (e.g. pilocarpine) may also provide this benefit, significant ocular and systemic effects arise with parasympathomimetic use, especially in phakic individuals. In PDS, pupillary mobility and contact of the posterior iris and the crystalline lens and zonules leads to shedding of iris pigment. Liberated granules may cause short- or long-term dysfunction of the TM and IOP dysregulation[34]. The limitation of pupillary mobility and induced miosis by brimonidine may be preferable in preventing pigmentary release and lowering IOP, also in lieu of parasympathomimetic agents which have been reported to carry an increased risk of retinal detachment in this population[38].
Pharmacological treatments available for the management of underactive bladder in neurological conditions
Published in Expert Review of Clinical Pharmacology, 2018
Seyedeh-Sanam Ladi-Seyedian, Behnam Nabavizadeh, Lida Sharifi-Rad, Abdol-Mohammad Kajbafzadeh
Although parasympathomimetic drugs have minor beneficial effects, the risk of frequent mild and rare serious side effects should be considered when these drugs are prescribed. Therefore, the unfavorable balance between minor benefits and considerable side effects suggests that parasympathomimetics should not be used routinely in clinical practice for UAB [67].
Related Knowledge Centers
- Acetylcholine Receptor
- Cholinesterase
- Glaucoma
- Nicotinic Acetylcholine Receptor
- Neurotransmitter
- Parasympathetic Nervous System
- Cholinergic
- Acetylcholine
- Agonist
- Muscarinic Acetylcholine Receptor