Acetyl cholinestrase inhibitor drugs potentiate the Ach which is synthesized by choline acetylase enzyme.

Wherever Ach is secreted these drugs will enhance Ach action. also blocked by botulism toxin. Indirect
acting cholinomimetics.

when a muscarinic m3 receptor activated in eye sphincter muscles miosis. ciliary muscles - accomodation
for near vision. too much will cause cyclospasm/plegia.

M2 in heart - nodal tissue. decrease in heart rate. negative ionotropic action.

everything else is m3 if not the heart except muscarinic receptor causing bronchospasm. Increases
secretion blocks airflow with too much acetylcholine. May get respiratory distress if too much , can give
muscarinic blocker in treatment of asthma and copd.

GI tract motility is increased by M3 RECEptors except M1 receptor responsible for secretion of acid.

contraction of bladder wall relaxation of all sphincter other than lower oesophageal sphincter.

Sweat glands have M3 receptor but innverated by sympathetic.

Glands in general salivation, lacrimation all muscarinic actions.

Blood vessels in endothelial cells have receptors which respond to Ach but no innervation there, there
can be done by nitric oxide or endothielial dilating factor but no nerves here remember.

Nicotinic receptors in adremal medulla, ganglia in ans branches. activation in adrenal medulla will
release catecholamine’s mainly epi some nor epi(neurohumoral transmission)

Purely endochondral : ETHyoiSt- Ethemoid, hyoid, stapes and incus.

Both endochondral and intramembranous: mandible; occipital, sphenoid and temporal.

Purely intramembranous: maxillary and nasal; frontal and parietal.

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