Adrenal medulla, nicotinic

Adrenal medulla Nicotinic Increased secretion of epinephrine and norepineprine —... 

Acetylcholine receptor Genistein Daidzein Bovine adrenal chromaffin cells Bovine adrenal medulla Nicotinic antagonist Nicotinic antagonist Matsumura et ah, 2007 Liu et ah, 2007c... 

Figure 9.2 Autonomic nerve pathways. All preganglionic neurons release acetylcholine (Ach), which binds to nicotinic receptors (N) on the postganglionic neurons. All postganglionic neurons in the parasympathetic system and some sympathetic postganglionic neurons innervating sweat glands release Ach that binds to muscarinic (M) receptors on the cells of the effector tissue. The remaining postganglionic neurons of the sympathetic system release norepinephrine (NE), which binds to alpha (a) or beta (P) receptors on cells of the effector tissue. The cells of the adrenal medulla, which are modified postganglionic neurons in the sympathetic system, release epinephrine (EPI) and NE into the circulation.

Pharmacology Nicotine, the chief alkaloid in tobacco products, binds stereo-selectively to acetylcholine receptors at the autonomic ganglia, in the adrenal medulla, at neuromuscular junctions, and in the brain. 

Endocrine Because of the action of nicotine on the adrenal medulla, use with caution in patients with hyperthyroidism, pheochromocytoma or insulin-dependent diabetes. 

In the adrenal medulla and the ganglia of parasympathetic and sympathetic nerves, the neurotransmission is mediated by acetylcholine. On the postsynaptic membranes the transmitter activates the neuronal-type of the nicotinic acetylcholine receptor. This receptor type is in fact a sodium channel, its activation leads to a sodium influx and a membrane depolarization. A pharmacological interference at the... 

Like in the neuromuscular junction the neurotransmission can be inhibited either by receptor blockade (non-depolarizing) or by overstimulation (depolarizing) of the receptors. The alkaloid nicotine, in low doses, stimulates ganglia and the adrenaline release from the adrenal medulla. High doses lead to a continuous depolarization of the postsynaptic membrane and thereby to an inactivation of the neurotransmission. All ganglion blockers in clinical use were synthetic amines of the nondepolarizing type trimethaphan, hexamethonium and mecamylamide. 

The administration of acetylcholine mimics the stimulatory effect of nicotine, the alkaloid from the tobacco plant, on autonomic ganglia and the adrenal medulla. It has become common practice to refer to the effects of acetylcholine on visceral effectors as the muscarinic action of acetylcholine and to its effects on the... 

In addition to autonomic ganglia, nicotinic receptors are found in a variety of organs, and their stimulation will produce quite different results in these different tissues. Activation of nicotinic receptors on the plasma membrane of the cells of the adrenal medulla leads to the exo-cytotic release of epinephrine and norepinephrine stimulation of nicotinic receptors at the neuromuscular junction results in the contraction of skeletal muscle (see... 

The effects of nicotine on the cardiovascular system mimic those seen after activation of the sympathoadrenal system, and they are principally the result of a release of epinephrine and norepinephrine from the adrenal medulla and adrenergic nerve terminals. These effects include a positive inotropic and chronotropic effect on the myocardium as well as an increase in cardiac output. In addition, both systohc and diastolic blood pressures are increased secondary to stimulation of the sympathoadrenal system. These effects are the end result of a summation of adrenergic and chohnergic stimulation. 

Schematic diagram comparing some anatomic and neurotransmitter features of autonomic and somatic motor nerves. Only the primary transmitter substances are shown. Parasympathetic ganglia are not shown because most are in or near the wall of the organ innervated. Cholinergic nerves are shown in blue noradrenergic in red and dopaminergic in green. Note that some sympathetic postganglionic fibers release acetylcholine or dopamine rather than norepinephrine. The adrenal medulla, a modified sympathetic ganglion, receives sympathetic preganglionic fibers and releases epinephrine and norepinephrine into the blood. ACh, acetylcholine D, dopamine Epi, epinephrine M, muscarinic receptors N, nicotinic receptors NE, norepinephrine.

Acetylcholine receptors are classified as either muscarinic cholinergic receptors or nicotinic cholinergic receptors. The alkaloid muscarine mimics the effects produced by stimulation of the parasympathetic system. These effects are postganglionic and are exerted on exocrine glands, cardiac muscle, and smooth muscle. The alkaloid nicotine mimics the actions of acetylcholine, which include stimulation of all autonomic ganglia, stimulation of the adrenal medulla, and contraction of skeletal muscle. 

Pet-1 is an ETS-domain transcription factor that was first discovered in adrenal chromaffin-derivd PC 12 cells, where it was found to induce transcription of the nicotinic acetylcholine 34 receptor (175). Pet-1 is expressed in the adrenal medulla as well as the eye and the brain (175) within the brain, it is expressed exclusively in serotonin neurons (176,177). Pet-1 expression appears... 

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. 

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. 

Nicotine binds selectively to the nicotinic receptors that are present in the adrenal medulla, brain, autonomic ganglia, and neuromuscular junctions. It causes the release of several neurotransmitters and hormones such as acetylcholine, norepinephrine, dopamine, serotonin, arginine vasopressin, j3-endorphin, adrenocorticotropic hormone, and cortisol (187). This neuro-regulatory effect of nicotine is dose-dependent and occurs as plasma nicotine level rises when tobacco is smoked. The neurotransmitters released in the brain medi-... 

---