week 6-L1 control of heart function Flashcards
what control the heart function?
CNS, blood vessel and kidneys
how CNS control of the heart
parasympathetic and sympathetic controls by ANS
CNS what does parasympathetic system do?
rest and digest therefore
decrease HR and slope of phase 4
CNS what does sympathetic system do?
increase HR and slope of phase 4
increase force of contraction and calcium dynamics
chronotropy
increase in heart rate
inotropy
increase in contraction force of ventricles from increase calcium dynamics
KIDNEY control of the heart
sympathetic innervation only- absence of parasympathetic innervation in the kidney
KIDNEY sympathetic control on heart
decrease glomerular filtration- decrease Na excretion
cause increase in blood volume and BP
KIDNEY blood volume regulation
detected by venous volume receptors
increase renin secretion- increasing angiotensin II production causing vasoconstriction- blood pressure increase
KIDNEY how is blood pressure detected?
arterial baroreceptors
BLOOD VESSEL cardiopulmonary circuit
volume sensors in atria and ventricles sending signals through the glossopharyngeal and vagus nerves
BLOOD VESSEL decrease in filling
detected by reduction in baroreceptors firing to increase SNS activity
BLOOD VESSEL distention
detected by increase in baroreceptors firing to increase the PNS activity and reduce SNS activity
features of PNS
pre and post ganglionic fibres release Ach as neurotransmitter and control heart rate
features on SNS
pre ganglionic fibres release Ach but post ganglionic fibres release noradrenaline
SNS important in controlling circulation
describe the mechanism SNS
beta-1 receptors activation cause Gs stimulation
AC activated converting ATP to cAMP to PKA
increase the HR and BP
describe the mechanism of PNS
M2 receptors cause the Gi stimulation that inhibits the conversion of ATP to PKA
reduction in HR and BP
what happens if SNS cut off
HR falls below normal
what happens if PNS cuts off
HR rise above normal
what does cut off CNS or PNS show
that both systems work together to maintain normal HR
renal system sympathetic fibre innervation
afferent and efferent arterioles
renal afferent arterioles effect of SNS
primary site of SNS activity
alpha 1 adrenoceptor causes vasoconstriction
decrease in glomerular filtration rate causes decrease in Na filtered
Juxtaglomerular cells site of renin synthesis, storage and release- beta 1 adrenoceptor stimulation cause renin secretion
designs of circulatory circulation and why
more blood % in vein and venues and less in arteries
increase preload and decrease after-load
constriction of veins and arteries
veins- causes reduction in compliance (ability to stretch0 and venous return decreasing preload
arteries- causes increase in after load as blood pressure increases
how to regulate blood flow
local and systemic mechanism
local mechanism of blood flow regulation
intrinsic smooth muscles or endothelial-derived mediators
vasodilators- nitric oxide on smooth muscles and prostacyclin anti platelet and anticoagulant effect
vasoconstrictors-thromboxane A2 heavily synthesised in platelets and endothelins from endothelial nucleus
systemic mechanism of blood flow regulation
extrinsic to smooth muscles and non derived endothelial mediators
vasodilators- kinins bind to receptor on endothelial cells and stimulate no synthesis and atrial natriuretic peptide response to stretch to reduce BP
vasoconstrictors- vasopressin binds to V1 receptors on smooth muscles, noradrenaline and angiotensin II stimulate ADH secretion
what increases atrial pressure?
blood volume, respiratory movements, SNS activation of veins and skeletal muscle pumps- increase venous pressure that in turn increase venous return
cardiac action potential features
longer action potential for longer slower contraction for more efficient pumping
5 phases ranging 0-4
Name the 5 phases of cardiac action potential
0- upstroke 1- early repolarisation 2- plateau 3- repolarisation 4- resting membrane potential
absolute refractory period
time lag during which no AP can be initiated independent of the stimulus intensity- phase 1 and 2
relative refractory period
period where an AP can be initiated follow ARP but required high stimulus intensity
what defines resting membrane potential
K+ influx
what defines upstroke
large increase in membrane to Na+
what defines contraction
Calcium influx which release calcium form intracellular store- L-type VGCC during plates phase
what defines the 100-200ms cardiac AP
gradual activation of K+ currents outwards balancing and overcoming calcium flow
NB large Ik inactive during plateau but increase once cells partially repolarised
Ik responsible for full repolarisation
what is the role of Ik
large and flows during diastole to stabilise the resting membrane potential
features of pacemaker (SAN) AP
presence of only phases 0,3,4
resting membrane potential become prepotential- can initiate another AP due to L-type VGCC and funny current
SNS effect on cardiac AP graph
chronotropy- cAMP activates If causing increase slope of phase 4 SAN
inotropy- increase calcium dynamics in myocytes
B1 receptor activation in renal afferent arterioles will have which initial effect?
secretion of renin
which receptor transmits signal from pre to post ganglionic nerves in the SNS?
nicotinic Ach receptor
when is the afferent nerve activity in the baroreceptor at its highest
high systolic blood pressure and pulse pressure
what effect will activation of renal alpha 1 receptor eventually have on the heart?
increased chronotropy and inotropy
