Summarise how the ANS works and what it consists of
- ANS consists of sympathetic and parasympathetic NS.
- They involve 2 synapse pathways - preganglionic + postganglionic (adrenal medulla - one long ganglionic nerve)
- SNS uses Ach as neurotransmitter and NA at the organ (some exceptions - sweat gland)
- PSNS uses only Ach at the ganglia and organ
Receptors - ANS
Cholinergic:
* Nicotinic
* Muscuranic (m1,m2,m3)
Adrenergic:
* Alpha (a1,a2)
* Beta (B1,B2,B3)
Drugs that increase/decrease nervous system function
- Sympathomimetic - increase/mimic NS function
- Sympatholytic - decrease/block NS function
same for PSNS
Do ANS drugs have specifcity, selectivity
ANS drugs show selectivity but not Specifity. So, a drug affecting one receptor subtype will interact/alter other recptor subtypes.
effects of parasympathomimetic drugs
- increased salivary/bronchial secretions
- increased peristalsis
- bronchoconstriction
- bradycardia/hypotension (low heart rate, low BP)
Large doses causes over stimulation
Pilocarpine
Parasympathomimetic
- used to treat glaucoma
- muscuranic acetylcholine receptor agonist
- eye drops cross conjunctival membrane
- pupilary constriction, reduction of intraoccular pressure
- side effects:
- allergic conjunctivitis, blurred vision, lid twitching
- nausea, vomitting, bradychardia, bronchoconstriction, hypotension
Bethanechol
parasympathomimetic
- selective mAchR - does not cross BBB
- Laxative (enhances parasympathetic activity therefore increased GI motility)
- rarely used due to side effects
- Side effects on bladder:
- hypotension/bradycardia
- increased GI motility/pain
- bronchconstriction
- increased salivation/sweating
muscuranic receptor agonist effects
Cardiovascular:
1. slowed heart beat
2. decreased cardiac output
3. decreased force of contraction
4. generalised vasodilation
- Smooth muscle:
- gastrointestinal
- detrusor constriction
- airway constriction
gland stimulation:
1. salivary
2. sweat
3. bronchial
4. pancreatic
5. gastric
Neostigmine
- increases availability of Ach to outcompete muscle relaxant (mr) therefore reversing effects of (mr)
- carbymalates the enzyme, which takes minutes to hydrolyse/reverse
AchE inhibitors
Donepazil - medium acting AchE inhibitor
* limited use due to adverse effects and so benifit must outweigh side effects
Side effects: nausea vomitting, increased GI motility, urinary incontinence, bradycardia
parasympathomimetic and CNS
mAchR antagonists
parasympaholytic
These drugs block the M receptors and so produce the oppisit effect of the mAchR agonists
effects:
dry mouth
gastric secretion
bronchial glands - mucus clearance inhibition
increased heart rate
reduced GI motility (constipation)
bronchodilation
urinary tract relaxation
Atropine
- antimuscarinic (mAchR antagonist)
- used to treat low heart rate by blocking m2 receptors increasing heart rate
Uses of antimuscarinics
- Asthma - short term releif of symptoms (bronchodilation)
- motion sickness - hyoscine
- parkinsons
Autonomic ganglia stimulants
- stimulates the nicotinic receptors found at the preganglionic neurones
- can produce excitatory and inhibitory depending on the receptor classes effected
side effects of autonomic ganglia stimulants
- gi disturbances
- dizziness
- flu like symptoms
- heart rate
cautions in:
cardiovascular disease
diabetes
peptic ulcers
autonomic ganglia blockers
- produce a bigger effect on SNS as blockage of these receptors = vasodilatory effect, as decreasing release of noradreneline
Adrenaline
*A&B adrenergic agonist
* caridac arrest - IV
* Anaphylactic shock - IM, IV emergency, EpiPEN
*Used with local anesthetics - allows LA to remain and work in that area for longer, also slowls rate of absorption and prolongs action
Alpha adrenergic agonists
- Vascular smooth muscle contraction
- Skin constriction
- veins, arteries constriction
- decreased vascular compliance
- decreased central venous pressure
- increased peripheral resistance
- increased BP initiates baroreceptor reflex
- cerebral/coronary/pulmanory beds unaffected
- INCREASED SYSTOLIC & DIASTOLIC BLOOD PRESSURE INCREASED CARDIAC WORK
- decongestants
types of a1 adrenergic agonists
a1:
* phenylephrine - contraction of nasal passages
a2:
* Clonidine
* antihypertension & migraine
* centrally acting hypertensive
* decreases cardiac output & peripheral resistance
* cannot withdraw treatment suddenly (hypersensative crisis)
Side effects:
* sedation
* depression
* fluid retention
* constipation
B receptor agonists
- works on smooth muscle
- relaxation
- GI tract relaxation
B adrenergic agonists
NT, H
Nerve terminals:
* presynaptic adrenoreceptors are found on both adrenergic and cholinergic nerves
* Main action: a2 adrenoreceptors inhibitory (main action)
* Weak action - B-adrenoreceptor facilitation
Heart:
* B1-adrenoreceptor powerful stimulant action on heart
* heart rate and force of contraction increased
* increased cardiac output and oxygen consumption
B adrenergic agonists
Metabolism:
B1,B2 adrenoreceptors located in the liver increase availability of glucose
B1 adrenergic agonist
Dobutamine:
* septic shock
* increased contractility
* IV administration
B2 adrenergic agonist
Salbutamol:
* bronchial smooth muscle dilated by the activation of B2 adrenoreceptors
* uterine smooth muscle dilated by the activation of the B2 adrenoreceptors
-can delay premature labour
