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Why do sympathomimetics make you sweaty if sweat glands have muscarinic receptors?

Answer:The Sympathetic NS regulates sweating (see table on page 81) by controlling the function of

about five million sweat glands in the body. There are two main types of sweat glands within the

body, both regulated by the sympathetic NS:

1. Cholinergic Sweat Glands: Thermoregulatory sweat glands throughout the body but they release

ACh and synapse with muscarinic receptors. 2. Adrenergic Sweat Glands: Nervous sweating on

palms, soles, and armpits and release NE and synapses with alpha1- (mostly) and some beta2-

receptors. A normal rise in body temperature is sensed by the hypothalamic center from which

stimuli emanate via sympathetic nerves to the sweat glands, resulting in appropriate sweating

(mainly cholinergic sweat glands ie release Ach). This serves to cool the body by the loss of heat

resulting from evaporation of the sweat, aided by a cool breeze. During stress or anxiety sweating

occurs mainly on palms and armpits (adrenergic sweat glands) through alpha1- and beta2-receptors.

A) are activated by acetylcholine

B) are located on the surface of ganglion cells in both the sympathetic and parasympatheticnervous systems

C) when stimulated always produce an excitatory response

D) control sodium channels in the affected membrane

E) are activated by norepinephrine

B)

Both A) and B) appear to be true, unless I am overlooking something...

Muscarinic receptors are G-protein linked receptors that are activated by acetylcholine. That makes

A) true.

Both nicotinic and muscarinic ACh receptors are located on the postganglionic cells in both the

sympathetic and parasympathetic nervous systems. However, neither ACh receptor is located on the

preganglionic cells of either the sympathetic or parasympathetic systems. So, since they are only

located on the post and not the pre, I would consider B) to be false.

Muscarinic receptors do not always produce an excitatory response. They are G-protein linked, so

they can cause a wide variety of activities within different cells. Nicotinic, on the other hand, always

involve the opening of a sodium channel and are therefore always excitatory. C) is false.

Nicotinic control sodium channels, so D) is false.

Norepinepherine does not activate ACh, so E) is false.

In my opinion, you could make an argument for either A) or B) being true. Muscarinic receptors are

located on the surface of ganglion cells in both the sympathetic and parasympathetic nervous

systems, but only on the postganglionic neurons. The ganglionic neurons only release ACh.

A) is therefore the "safe" choice.

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Im having a bit of trouble getting my head around this for exams...

So nicotinic and muscarinic receptors are both cholinergic receptors? Does this mean Ach is the part

that binds to the receptors, and if yes does it bind to both the nicotinic and the muscarinic, or are

there different ones?

And...a muscarinic agonist is something (substance/toxin) that causes the muscarinic receptor to be

over-stimulated, so does this mean that whatever this substance may be, it binds to the receptor

even tho its not Ach, therefore causing all of the side effects of over stimulation, eg emesis, GIT

motility, salivation...

And a muscarinic ANTagonist is something that slows down the 'receptibility' of the receptors, so if

someone was exposed to a muscarinic agonist, could an antagonist be given to reverse the effects?

And what would happen if the body was only exposed to a muscarinic antagonist?

And would an inhibited nicotinic receptor cause paralysis?

Thankyou so much in advance!

Tried to answer the specific questions you asked.

1) Yes they both bind to acetylcholine but work in two different ways (one is an ligand-gated ion

channel, the other is a 7 domain g-coupled protein receptor with a secondary messenger system).

2) Yes it does bind to both of these receptors (but they are not found together- one is post synaptic

the other is on the effector organ/tissue)3) An agonist just stimulates the receptor (this doesn't mean that it must over-stimulate the

receptor), an antagonist prevents receptor stimulation. Some agonists are only partial agonists and

do not produce a "good" response.

4) Many toxins work by "blocking" or antagonising the muscarinic receptor and cause paralysis. So

yes depending on what drug you inject the result will be stimulation or inhibition.

5) Antagonists do not give the reverse effect they just do not produce a response. They have

receptor affinity but can not cause activation and produce a reaction.

6) Like toxins a muscarinic antagonist would most likely cause paralysis.

7) inhibiting just one receptor won't do anything but mass inhibition will.

Hope this helps