Simultaneous Studies of the Effect of Various Cholinergic and Anticholinergic Drugs on End Organs of the Autonomic Nervous System: Stomach, Colon, and Urinary Bladder

1957 ◽  
Vol 77 (2) ◽  
pp. 214-220 ◽  
Author(s):  
John W. Draper ◽  
Mieczyslaw Sierp ◽  
Oswaldo Karam
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Urinary Bladder ◽  
Anticholinergic Drugs ◽  
Autonomic Nervous

Consultation with the Specialist

1994 ◽  
Vol 15 (10) ◽  
pp. 389-390
Author(s):  
Stephen C. Hardy ◽  
Allan Walker
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Neuromuscular Junction ◽  
Parasympathetic Nervous System ◽  
Anticholinergic Drugs ◽  
Entire Body ◽  
Gi Tract ◽  
Cholinergic Activity ◽  
Gallbladder Contraction ◽  
Autonomic Nervous

Acetylcholine (ACh), a common neurotransmitter in the human, acts in the brain at the neuromuscular junction and throughout the autonomic nervous system. Cholinergic receptors have been separated into two main groups: nicotonic (present at the neuromuscular junction) and muscarinic (present at all ganglia of the autonomic nervous system and postsynaptically in the parasympathetic nervous system). Anticholinergic medicines act at muscarinic sites. The first anticholinergic drugs were extracts of belladonna plants, which were used for centuries for their antimotility and antisecretory properties. These drugs generally are ineffective blockers of ACh at nicotinic receptors and cause neuromuscular blockade only at excessive doses. Because antimuscarinic medications block the effect of the parasympathetic nervous system, they affect the gastrointestinal (GI) tract. In general, the parasympathetic nervous system stimulates the GI system. Cholinergic impulses cause increased tone and motility of the stomach and intestines and increased secretion of gastric and intestinal fluids. Exocrine pancreatic secretion and gallbladder contraction also are stimulated by cholinergic activity. Anticholinergics reverse these responses. The prototypical anticholinergic, atropine, decreases output of gastric, intestinal, and pancreatic secretions; decreases motility and tone of the GI tract; and relaxes the gallbladder. Atropine not only interferes with cholinergic activity in the GI tract, it affects the entire body increasing heart rate, depressing salivary and bronchial secretion, decreasing sweating, dilating the pupils, inhibiting accommodation, inhibiting micturition, and causing constipation.

Influence of the autonomic nervous system in the horse urinary bladder

1988 ◽  
Vol 44 (3) ◽  
pp. 282-285 ◽  
Author(s):  
A. LABADIA ◽  
L. RIVERA ◽  
G. COSTA ◽  
A. GARCIA-SACRISTAN
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Urinary Bladder ◽  
Autonomic Nervous

scholarly journals The Ameliorating Effect of Exogenous Melatonin on Urinary Bladder Function in Hyperosmolar Bladder Overactivity and its Influence on the Autonomic Nervous System Activity

2011 ◽  
Vol 54 (2) ◽  
pp. 63-68 ◽  
Author(s):  
Kajetan Juszczak ◽  
Agata Ziomber ◽  
Anna Machowska ◽  
Agata Furgała ◽  
Łukasz Dobrek ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Urinary Bladder ◽  
Bladder Capacity ◽  
Bladder Function ◽  
Melatonin Treatment ◽  
Motility Index ◽  
Group Iii ◽  
Autonomic Nervous ◽  
Bladder Activity

This study was designed to investigate the effects of melatonin on the bladder hyperactivity in hyperosmolar-induced overactive bladder (OAB) rats. Additionally, the influence of melatonin on the autonomic nervous system (ANS) using heart rate variability (HRV) analysis was assessed. 40 rats were divided into four groups: I – control (n=12), II – rats with hyperosmolar OAB (n=6), III – rats with melatonin pretreatment and hyperosmolar OAB (n=6) and IV – control with melatonin pretreatment (n=6). In group III and IV melatonin in dose of 100 mg/kg was given. HRV measurements in 10 rats, as follow: control (n=2), control after melatonin treatment (n=2), rats with hyperosmolar OAB without (n=3), and after (n=3) melatonin treatment were conducted. This study demonstrates marked influence of melatonin on urinary bladder activity in hyperosmolar-induced OAB rats. These rats showed significantly reduced the detrusor motor overactivity resulting in the improvement of cystometric parameters after melatonin treatment when compared to the control, as follow: a significant increase of intercontraction interval (70 %) and functional bladder capacity (67 %), as well as a decrease of the basal pressure, detrusor overactivity index and motility index of 96 %, 439 % and 40 %, respectively. ANS activity analysis revealed sympathetic overactivity in OAB rats, and parasympathetic superiority in melatonin treated OAB rats. Melatonin treatment in rats with hyperosmolar OAB (group III) caused significant increase of nuHF parameter (from 51.00 ± 25.29 to 76.97 ± 17.43), as well as a decrease of nuLF parameter (from 49.01 ± 25.26 to 23.03 ± 17.43) and LF/HF ratio (from 1.280 ± 0.980 to 0.350 ± 0.330). In conclusion, melatonin suppresses hyperosmolar OAB, and modulates ANS activity by inhibition of the sympathetic drive. Therefore, melatonin may become a useful agent for OAB management.

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