14 –Autonomic Nervous System Flashcards
NTs: somatic nerves
- ACh: nicotinic receptor
Receptors in ganglia are always
- Nicotinic
NTs: preganglionic nerve onto adrenal medulla
- ACh: nicotinic receptor
o E+NE released into blood
NTs: pre-ganglionic sympathetic nerves
- ACh: nicotinic
NTs: post-ganglionic sympathetic nerves
- NE
o Heart: beta-1
o Smooth muscle : alpha-1,
E from the blood: beta-2
NTs: pre-ganglionic parasympathetic nerves
- ACh: nicotinic
o Exocrine glands: M3
o Heart: M2
o Smooth muscle : M3
NTs: post-ganglionic PS nerves
- ACh
Sympathetic NS: ‘spinal segments’
- Preganglionic nerves exit spin in thoracic and lumbar nerves
- Sympathetic chain ganglion: synapses above and below
o *Responses tend to be ALL OR NONE!
Parasympathetic NS: ‘spinal segments’
- Cranial and sacral nerves
- Longer pre-ganglionic neuron
- Ganglion may be in the ‘target organ/tissue’
- Discrete activation
o Can get one nerve activated without activated another - *vagus is major player
Baroreceptor reflex
- Increased arterial pressure=stretch of baroreceptors in aortic arch and carotid artery
- Vasomotor center:
a. Decreased sympathetic impulses on arterioles=vasodilation
b. Increase PS impulses mainly on heart=decrease HR= decrease CO=decrease BP
Agonist is
- Substance that binds to a receptor and activates it
- Can be an exogenous chemical (drug)
- Mimics actions of an endogenous ligand
Antagonist is
- Substance that binds to a receptor, but prevents its activation
- Blocks effects of drugs that activate the receptor
- Blocks effects of endogenous activators of a receptor
PS vs S
- Effects generally oppose each other (physiological systems that antagonise each other)
- One system will have predominant ‘tone’ over the other in a given organ
o Resting: PS should be predominant (exception: arterioles) - Blocking one system often UNMASK activity of opposing system
Arterioles
- Main controller of BP
- Have no PS innervation!
- Control BP through S innervation degree of activity
ACh cholinergic receptors: 2 major subtypes
- Muscarinic: M1-M5
- Nicotinic: Nm (skeletal muscle), Nn (neurons: ganglia or adrenal medulla)
Muscarinic receptors and drugs
- Don’t have any drugs that aren’t toxic
- *’dirty’: hit everything
o Usually many side effects
NE and E adrenergic receptors: 2 major subtypes
- Alpha-adrenergic: a1, a2
- Beta-adrenergic: b1, b2, b3
Beta-3
- On many cells
o adipocyte cells! (obesity) - Drugs for anti-obesity?
Effects of IV infusion of NE at low to moderate dose
- Increase in pulse pressure
- Marked increase in peripheral resistance
- Increase in systolic BP
- increase in diastolic BP
- *no increase in pulse rate as baroreceptor response
Beta-1 adrenergic antagonist in a resting animal:
- Decrease HR
- Decrease force of contraction in heart
- *vagal stimulation pre-dominates
Beta-1 adrenergic antagonist in an agitated animal
- Have significant sympathetic stimulation
o *beta-blocker will slow HR and reduce contractility
ANS receptor signal transduction
- Beta-receptor (M3) activates Gs which stimulates adenyl cyclase=more cAMP=more PKA=effect
- Alpha 2 and M2 receptors (heart)=activate Gi which inhibits adenylyl cyclase=less cAMP=decrease PKA=decreased biological effect
How do you turn cAMP ‘off’?
- Phosphodiesterase to get AMP
- *if inhibit phosphodiesterase=get more cAMP=more biological effect
- *same with cGMP
Vascular endothelium and NO
- M3-receptor on endothelium stimulated=activate IP3, DAG=Ca2+ and Ca-calmodulin and get NO
o Short lived
o Some into lumen of artery
o LOTS diffuses into vascular smooth muscle cell - Muscle cell: stimulates guanyly cyclase=get cGMP=relaxation!
- *Viagra prefers to work on this phosphodiesterase=get more dilation