Ganglia nicotine action

Nicotinic signs of intoxication include muscle weakness, tremor and fasciculations, and involuntary twitching. Muscle weakness that affects the respiratory muscles may contribute to dyspnea and cyanosis. Tachycardia may result from stimulation of sympathetic ganglia in cardiac tissue and may mask the bradycardia due to the muscarinic action on the heart. Nicotinic action at the sympathetic ganglion may also result in pallor, high blood pressure, and hyperglycemia. 

Actions Carbachol has profound effects on both the cardiovascular system and the gastrointestinal system because of its ganglion-stimulating activity and may first stimulate and then depress these systems. It can cause release of epinephrine from the adrenal medulla by its nicotinic action. Locally instilled into the eye, it mimics the effects of acetylcholine, causing miosis. 

The hypertension which tyramine causes is attributed, as that of hordenine, to its nicotinic action on sympathetic ganglia (170). Raymond-Hamet observed a ganglionic paralysis under the influence of tyramine (188). 

Nicotinic mechanism The mechanism of nicotinic action has been clearly defined. The ACh receptor is located on a channel protein that is selective for sodium and potassium. When the receptor is activated, the channel opens and depolarization of the cell (an excitatory postsynaptic potential EPSP) occurs as a direct result of the influx of sodium. These ACh receptors are present on ganglion cells (both sympathetic and parasympathetic) and the neuromuscular end plate. If large enough, the EPSP evokes a propagated action potential in the surrounding membrane. 

Atropine blocks muscarinic receptors and inhibits parasympathomimetic effects. Nicotine can induce both parasympathomimetic and sympathomimetic effects by virtue of its ganglion-stimulating action. Hypertension and exercise-induced tachycardia reflect sympathetic discharge and therefore would not be blocked by atropine. The answer is (E). 

Hexamethonium (Fig. 16.28) is a quaternary ammonium agent. It was the first successful antihypertensive treatment. However, its side effects led to discontinuation of its use. It is thought to exert its action by blocking the ion channel rather than the acetylcholine active site. Blocking the ganglionic nicotinic receptor will stop the... 

At a low concentration, the tobacco alkaloid nicotine acts as a ganglionic stimulant by causing a partial depolarization via activation of ganglionic cholinocep-tors (p. 108). A similar action is evident at diverse other neural sites, considered below in more detail. 

So, parasympathetic nerves use acetylcholine as a neurotransmitter and cholinomimetic drugs mimic the action of acetylcholine at its receptors. Muscarinic receptor subtypes are found on neuroeffector junctions. Nicotinic receptor subtypes are found on ganglionic synapses. Chohnomimetics can be classified as ... 

The basis for the antihypertensive activity of the ganglionic blockers lies in their ability to block transmission through autonomic ganglia (Fig. 20.2C). This action, which results in a decrease in the number of impulses passing down the postganglionic sympathetic (and parasympathetic) nerves, decreases vascular tone, cardiac output, and blood pressure. These drugs prevent the interaction of acetylcholine (the transmitter of the preganglionic autonomic nerves) with the nicotinic receptors on postsynaptic neuronal membranes of both the sympathetic and parasympathetic nervous systems. 

Lobelia is a nicotine-like herb that acts as an agonist at the nicotinic ganglion. Consistent with this action, it can be dangerous in an overdose, causing respiratory distress, rapid heart rate, sweating, decreased blood pressure, convulsions, and coma. As a result, the FDA has declared it to be an unsafe herb ( 238). 

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