Parasympathetic depressants

Homatropine methylbromide is transported poorly aens-the blood-brain barrier because of its quaternary ammonium group and, therefore, has far fewer stimulant properties than atropine. It does have all the characteristic peripheral parasympathetic depressant propterties of atropin and is u.sed to reduce oversecretion and to relieve GI spasms. 

Tropane alkaloids L-Hyoscyamine, atropine (D 17.2) Parasympathetic depressant, spasmolytic... 

Hyoscamine acts on tissue cells innervated by post-ganglionic cholinergic fibres of the parasympathetic nervous system it is antimuscarinic and a parasympathetic depressant. 

With the knowledge of the action of the sympathetic and parasympathetic autonomic systems, one can understand the action of certain drugs. When acute diarrhea is encountered, sympathetic-type drugs or parasympathetic depressant drugs are often used. Drugs that act as parasympathetic stimulators are frequently used as laxatives. 

General types of physiological functions attributed to quaternary ammonium compounds are curare action, muscarinic—nicotinic action, and ganglia blocking action. The active substance of curare is a quaternary that can produce muscular paralysis without affecting the central nervous system or the heart. Muscarinic action is the stimulation of smooth-muscle tissue. Nicotinic action is primary transient stimulation and secondary persistent depression of sympathetic and parasympathetic ganglia. 

Since the main clinical use for antisympathotonics is in the treatment of essential hypertension, such drugs will be discussed in Chapter 20 in more detail. The alkaloid reserpine from Rauwolfia serpentina was the first drug used clinically to reduce sympathetic tone. Reserpine reduce the ability of storage and release of various transmitters (adrenaline, noradrenaline, serotonine and dopamine) by an irreversible destruction of the axonal vesicle membranes. The duration of the reserpine effect is actually determined by the de novo synthesis of these structure. Beside various central side effects like sedation, depression, lassitude and nightmares the pattern of unwanted effects of reserpine is determined by the shift of the autonomic balance towards the parasympathetic branch myosis, congested nostrils, an altered saliva production, increased gastric acid production, bardycardia and diarrhea. As a consequence of the inhibition of central dopamine release, reserpine infrequently shows Parkinson-like disturbances of the extrapyramidal system. 

In comparison with more modem antihypertensives reserpine causes unpleasant side-effects, such as sedation, depression and various effects reflecting a dominant parasympathetic system (nasal congestion, diarrhea and exacerbation of peptic ulcers). Reserpine should be considered as an antihypertensive of second choice, although in certain countries it is still used because of its low price. 

Severely depressed conduction may result in simple block, eg, atrioventricular nodal block or bundle branch block. Because parasympathetic control of atrioventricular conduction is significant, partial atrioventricular block is sometimes relieved by atropine. Another common abnormality of conduction is reentry (also known as "circus movement"), in which one impulse reenters and excites... 

NPY produces a variety of central nervous system effects, including increased feeding (it is one of the most potent orexigenic molecules in the brain), hypotension, hypothermia, respiratory depression, and activation of the hypothalamic-pituitary-adrenal axis. Other effects include vasoconstriction of cerebral blood vessels, positive chronotropic and inotropic actions on the heart, and hypertension. The peptide is a potent renal vasoconstrictor and suppresses renin secretion, but can cause diuresis and natriuresis. Prejunctional neuronal actions include inhibition of transmitter release from sympathetic and parasympathetic nerves. Vascular actions include direct vasoconstriction, potentiation of the action of vasoconstrictors, and inhibition of the action of vasodilators. 

N.A. Terpenes, sesquiterpenes, aplotaxene, sausarine, resin." Depress the parasympathetic nervous system. 

In the unanesthetized dog, reserpine selectively depresses the sympathetic centers and induces facilitation of the parasympathetic centers in the diencephalon. The latter effect accounts for the bradycardia, miosis, aggravation of bronchial asthma, renal and biliary colic, and ulcerative colitis observed in some patients receiving the drug. 

OPs and carbamates have different receptor activities in the mammalian nervous system. OPs have effects on muscarinic and nicotinic receptors and can cause neurological effects in the CNS (Levy-Khademi et al., 2007). Carbamates are thought to cause only parasympathetic muscarinic effects with limited nicotinic and CNS effects (Sofer et al, 1989). However, there are case reports in children that have revealed the presence of CNS effects with carbamate exposures (de Tollenaer et al, 2006). One pediatric case series stated that the signs and symptoms from carbamate poisoning were indistinguishable from OP exposures, with severe CNS depression with stupor and coma occurring in eight cases (Sofer et al, 1989). 

Any amount of heroin can be potentially toxic, especially when the purity of this illicit drug is not known. Heroin depresses the CNS, thereby producing coma and respiratory depression. Pulmonary edema has been described following heroin overdose. Respiratory arrest may occur. Miosis is often present but may be absent in the presence of hypoxia or mixed drug over doses. With depression of the CNS, there is also a decrease in sympathetic tone and an increase in parasympathetic tone. This yields bradycardia and hypotension. Hypothermia may also occur as a result of peripheral vasodilation. Urine can be screened for heroin metabolic products. Blood heroin levels are not clinically useful. 

The specific mechanism of toxicity of kerosene has not been completely determined. The primary risk from ingestion of kerosene is aspiration during emesis, which may cause pneumonitis. The biochemical mechanism of lung response to large concentrations of aerosolized kerosene (resulting in bronchocon-striction and asthma-like symptoms) may involve the parasympathetic nervous system via a direct effect on the vagus nerve or by inhibition of acetylcholinesterase. The mechanism(s) of central nervous system (CNS) depression from kerosene exposure has not been elucidated, but undoubtedly includes disruption of the membranes of nerve cells. 

Tobacco smoke includes 4000 chemical species with varying potential which cause adverse effects. Nicotine is stimulating to the autonomic nervous system ganglia and neuromuscular junction. The most prominent effects relate to stimulation of the adrenal medulla, central nervous system (CNS), cardiovascular system (release of catecholamines), gastrointestinal tract (parasympathetic stimulation), salivary and bronchial glands, and the medullary vomiting center. There is subsequent blockade of autonomic ganglia and the neuromuscular junction transmission, inhibition of catecholamine release from the adrenal medulla, and CNS depression. 

The parasympathetic branch of the autonomic nervous system (see 15.1 The Nervous System) depresses a response using adrenergic blockers (sympatholytics) that block the norepinephrine response at the adrenergic receptor sites (see Table 15.2). 

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