1. Parasympathetic agonist & antagonist
Muscarinic antagonist or Antimuscarinic drug
Parasympatholetic agents
Same effect sympathic system
Muscarinic agonist
cholinomimetics agents
Parasympathomimetic agents
Same effect of Parasympathic system
examples:
Atropine , Scopolamine(hyosine) , Ipratropium , Pirenzepine
Effect on each organ or system :
A. CNS:
Atropine in therapeutic doses has a minimal stimulant effect on CNS and a slower-long lasting sedative = drowsiness effect on the brain
Scopolamine has more marked CNS effects producing drowsiness in recommended doses
BOTH In HIGHR DOSES: agitation, excitement, hallucination and coma
B. Eye
Mydriasis= pupil dilation
Relaxation of ciliary muscle=Cycloplegia (plegia =paralysis) leads to loss of accommodation(eye can not focus on near objects) u need to see far object so u can run and hide
Reduction of lacrimal secretion, dry eyes
C. Cardiovascular system
Heart: The initial effect is bradycardia followed by tachycardia
bradycardia= slow heart rate :HOW?
blockade of presynaptic M1 muscarinic receptors = Ach leakage
Tachycardia= High heart rate: HOW?
blockade of M2 receptors on the heart = more Ach will effect the contraction of the heart
B.Vs : Inhibition of vasodilation = antagonist block M3
Vasodilation induced by cholinomimetics.
*هذي تخلي الأوعية الدمية زي ماهي يعني ما تسوي vasoconstriction
D- Respiratory system
bronchodilation
Antimuscarinic drugs are added to general anesthetics to reduce secretion in the trachea
Examples:
Effect on each organ or system
A. CNS:
excitatory neurotransmitter in the basal ganglia =increased locomotor activity tremor=الرعشة
B. Eye
contraction of the smooth muscle of the iris causing miosis= Pupil constriction
contraction ciliary muscle=accommodation of near vision= like when u read u need to see clearly near words
outflow of aqueous humor into the canal of Schlemn , drains the anterior chamber
C. Cardiovascular system
Heart: Heart rate (-ve chronotropy= slow heart rate), Bradycardia
conduction velocity , refractory period
B.Vs : BP >HOW? Due to Bradycardia and vasodilation?> Muscarinic agonist attached on M3 receptor on B.Vs causes release of NO(vasodilation agent) that’s will lead to : vasodilation that will lead to drop in BP
D- Respiratory system:
Bronchio-spasm = bronchoconstuction
increase secretion

2. Parasympathetic agonist & antagonist continued…..
E. Exocrine gland
Increased their secretion, sweating, lacrimation and salivation
F. GIT
secretions mainly salivary(wet mouth)
GIT motility
Gastric secretion
peristalsis الحركة الدودية بالأمعاء
Sphincters are relaxed
G.GU:
Stimulation of detrusor muscle(covers the bladder)
and Relaxation of the trigone and sphincter of the bladder thus promote micturition.
A)NMJ
Application of nicotine agonist in NMJ leads to depolarization of the endplate
The response vary from fasciculation of independent motor units to a strong contraction of entire motor unit.
B)Peripheral nervous system
Activation of nicotinic receptors in the autonomic ganglia result in firing action potential in postganglionic neurons
The action is same on both sympathetic and parasympathetic ganglia
E.sweat glands
Sweat gland secretions are blocked by antimuscarinic drugs, > thermoregulation is suppressed leading to increase in body temperature.
F. GIT
marked reduction in salivary secretion (dry mouth)
Gastric secretion is blocked less effectively? > not controlled by parsympathic also there r hormones control Gastric secretion
G.GU:
Smooth muscle of the uterus is relaxed
Inhibition of detrusor muscle(covers the bladder)
Bladder wall is relaxed and voiding(micturition) is slower
A) neuromuscular blockers :
1- depolarizing NMJ blocking drugs; the depolarizing blockers first depolarize the motor end-plate and then prevent further depolarization. E.g. Succinylcholine
2- non-depolarizing NMJ blocking drugs; compete with acetylcholine for receptors at the neuromuscular junction and clinical relaxation begins when 80–85% of the receptors on the motor end-plate are blocked. tubocurarine
B) Ganglion blocking drugs can occur by several mechanisms:
By interfering with Ach release
By prolonged depolarization due to large dose of stimulation = depolarizing
By interfering with postsynaptic action of Ach.= non-depolarizing
Nicotinic agonists & antagonist continued…..
Nicotinic antagonist
Nicotinic agonists