Session 5 - Autonomic control of CVS and BP Flashcards
recap - arrangments of ganglions in the ANS
Sympathetic - short preganglion - long postganglion to target tissue
parasympathetic - long pre ganglion then a short post ganglion innervated in the target tissue
what is the role of the sympathetic system on the heart? what receptors does it act on ?
will lead to increased heart rate and a greater force of contraction by acting on the B1 receptors
what is the role of the parasympathetic system on the heart? what receptors does it act on ?
it will decrease the heart rate by acting on the M2 muscarinic receptors
bonus : sympathetic drive to different tissues are independently regulated
what does the ANS control of the ANS
ANS controls heart rate and force of contraction and TPR but not initaite the heart beat , SA node does this
draw a diagram of the heart that shows ANS input to the heart, with receptors and nerves ect
check against lecture 10
how does the ANS effect the pacemaker potential of the SA node ?
sympathetic via the B1 receptors will increase pacemaker potential - noradrenaline binds and increase cAMP via a Gas GPCR - activates PKA - more phosphorylation of ca2+ channels - more Ca2+ enters myocardium - increases the force of contraction
Parasympathetic will decrease the pacemaker potential via M2 receptors - Gai GPCR will decrease cAMP
what is the effect of the ANS on vasculature ?
it may help to draw this
ANS in only innervated by sympathetic nerves !!!
they have a1 adrenoreceptors - vasodilation is caused by a decrease in sympathetic output, and vasconstriciton by an increase in sympathetic out put of NA
some vessels also have B2 adrenoceptors
physiological conc - adrenaline binds to B2 and cause vasodilation - increase cAMP —> PKA , opens K+ channels and inhibits MLCK to stop contraction
at pharmocological conc - it will also acitvate A1 receptors to cause vasoconstriction
- stimulates IP3 pathway - more Ca2+ influx - prolonged contraction
what is the more important trigger of vasodilation ?
active tissue will produce metabolites such as K+, H+, Adenosine and CO2
this has a very strong vasodilator affect
they are more important than B2 receptors
outline how barorecptors work
aortic arch and carotid sinus - stretch to trigger AP - this singals to brain an increase in arterial pressure
this causes brain to trigger bradycardia and vasodilation to counteract this
it is the most important in maintaining BP over SHORT TERM by altering cardiac output
baroreceptors can set to higher levels with a persistent increase in BP - hypertension
briefly outline drugs that act on the ANS
just the outline, not the detail
Sympathomimetics
• cardiovascular uses
– administration of adrenaline to restore function in cardiac arrest
– β1 agonist - dobutamine may be given in cardiogenic shock (pump failure)
– adrenaline administered for anaphylactic shock
Adrenoreceptor antagonists • α-adrenoreceptor antagonists – α1 antagonists eg prazosin – anti-hypertensive agent • inhibits NA action on vascular smooth muscle α1 receptors - vasodilation
• β-adrenoreceptor antagonists
– propranolol
• non-selective β1/β2 antagonist
• slows heart rate and reduces force of contraction (β1) but also acts on bronchial smooth muscle (β2) - bronchoconstriction
Cholinergics
• Muscarinic agonists
• Muscarinic antagonists
– increases heart rate, bronchial
dilation
what is hypertension ?
give values for normal and hypertensive BP values
hypertension is a sustained high BP
normal range 90/60mmhg - 120/80
stage 1 more than 140/90
stage 2 more than 160/100
severe hypertension more than 180/110
what are the causes of hypertension ?
95% primary hypertension - cause unknown
secondary hyper tension - we know cause and treat by treating the underlying cause
renovascular disease
chronic renal disease
chushings and conns syndrome
hypertension can cause heart failure, MI, Stroke, reniopathy, renal failure, LV hypertrophy
draw a diagram explaining the consequences of hypertenison and what causes each thing
check lecture 11
the baroreceptor refelx controls short term BP changes
how do we control BP in the long term
general idea is by controlling the sodium balance and hence control the extracellular fuild volume that will follow the Na+ conc
what are the 4 pathways that you need to know that control cirvulating volume and hence BP
- renin-angiotensin-aldosterone system
- sympathetic nervous system
- Antidiuretic Hormone (ADH)
- Atrial Naturetic Hormone (ANP)
outline how the renin-angiotensin-aldosterone system works ?
Not vital
- Renin is released from granular cells of juxtaglomerular apparatus (JGA)
- Factors that stimulate renin release:
a) Reduced NaCl delivery to distal tubule
b) Reduced perfusion pressure in the kidney causes the release of renin detected by baroreceptors in afferent arteriole
c) Sympathetic stimulation to JGA increases release of renin
draw the angiotensin system and what acts on it , and what it acts on
also include drugs and where they target
check against lecture 11
angiotensin II will go on to cause vasoconstriction, Simulate Na+ (water) resoprtion from the kindey and stimulate aldosterone release from adrenal cortex, which also Simulates Na+ (water) resorption from the kindey, increase thirst sensation - all this is triggered by AT1 and AT2 - angiotensin receptors
how does the sympathetic nervous system alter BP ling term ?
High levels of sympathetic stimulation reduce renal blood flow
– Vasoconstriction of arterioles
reduce renal blood flow - decrease Na+ excretion
• Stimulates renin release from JGcells
– leading to increased Ang II levels
– leading to increased aldosterone levels
• increased Na+ reabsorption
how does Antidiuretic Hormone (ADH) alter BP long term ?
• Main role is formation of concentrated urine by retaining water to control plasma osmolarity
– Increases water reabsorption in distal nephron
how does Atrial Naturetic Hormone (ANP) alter BP long term
Atrial natriuretic peptide (ANP) promotes Na+ excretion
• synthesised and stored in atrial myocytes
• released from atrial cells in response to stretch
– reduced filling of the heart – less stretch – less ANP released - BP can increase again
ANP causes vasodilation, inhibts Na reabsorption
how do we treat hypertension ?
non pharma approach
diet
excercise
low Na+ diet
reduce alcohol
Drugs
ACE inhibtors
ANG II receptor agonists/blocker
vasodilators
beta blockers - when other issues as well
