Acetylcholine urinary effects

Antagonists of muscarinic acetylcholine receptors had widely been used since 1860 for the treatment of Parkinson s disease, prior to the discovery of l-DOPA. They block receptors that mediate the response to striatal cholinergic interneurons. The antiparkinsonian effects of drugs like benzatropine, trihexyphenidyl and biper-iden are moderate the resting tremor may sometimes respond in a favorable manner. The adverse effects, e.g., constipation, urinary retention, and mental confusion, may be troublesome, especially in the elderly. 

Mechanism of Action A G1 ant ispasmodic and ant ichol inergic agent that inhibits the action of acetylcholine at postganglionic (muscarinic) receptor sites. Therapeutic Effect Decreases secretions (bronchial, salivary, sweat gland) and gastric juices and reduces motility of G1 and urinary tract. 

Mechanism of Action A quaternary ammonium compound that has anticholinergic properties and that inhibits action of acetylcholine at postganglionic parasympathetic sites. Therapeutic Effect Reduces gastric secretions and urinary frequency, urgency, and urge incontinence. 

Mechanism of Action A urinary antispasmodic t hat act s as a direct antagonist at muscarinic acetylcholine receptors in cholinergically innervated organs. Reduces tonus (elastictension) of smooth muscle in the bladder and slows parasympathetic contractions. Therapeutic Effect Decreases urinary bladder contractions, increases residual urine volume, and decreases detrusor muscle pressure. 

It is effective orally and resistant to pseudo-cholinesterase and possesses longer duration of action. Its nicotinic action is less than acetylcholine and actions are more marked on CVS as compared to GIT and urinary system. Earlier it was used for CVS disorders such as peripheral vascular disease and paroxysmal supraventricular tachycardia. But now, it is rarely used in therapeutics. 

Antimuscarinic effects Blockade of acetylcholine receptors leads to blurred vision, xerostomia (dry mouth), urinary retention, constipation, and aggravation of glaucoma and epilepsy. 

In addition to the more or less standard actions of anticholinergic compounds due to their ability to interfere with the actions of acetylcholine on muscarinic receptors (resulting in acceleration of the heart relaxation of smooth muscles in bronchi and bronchioles, intestinal tract, urinary tract, iris and ciliary body of the eye, bile ducts and gall bladder, and some cutaneous blood vessels and decrease or abolition of secretion by glands of the gascrolncesclnal tract and skin), these substances may have pronounced effects on the central nervous system, as has been mentioned earlier. A large amount of research with experimental animals has been directed toward elucidation of the basic mechanisms Involved in these actions. 

Carbachol is a quaternary ammonium compound that shares both the muscarinic and nicotinic actions of acetylcholine but is much more slowly deactivated. Carbachol has been used topically in ophthalmology and systemically (subcutaneously, for example in doses of 2 mg/day) for urinary retention. Severe cholinergic effects can result. In one instance they primarily involved the gastrointestinal tract and the patient died of esophageal rupture (1). In other cases patients have experienced extreme bradycardia with hypotension, requiring treatment with intravenous atropine. As carbachol is not destroyed by cholinesterase, a cumulative effect is possible in patients who receive regular doses at short intervals in one case, hypotension only developed on the third treatment day (2). 

Muscarinic effects, mediated by acetylcholine, the primary transmitter of the autonomic nervous system ganglia, are inhibited by the anticholinergic effects exerted by antihistamines. Anticholinergic side effects include dry mouth, urinary retention, blurred vision, and constipation. Because first-generation antihistamines also distribute into the CNS, sedation is a prominent side effect. The development of second-generation antihistamines, such as loratadine and fexofenadine, lack anticholinergic activity and do not distribute into the CNS (Table 31-1). Hence, they are not typically associated with sedation and do not possess antiemetic properties. 

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