BP regulation Flashcards
what factors is blood pressure dependent on>
HR, size and flexibility of arteries, force and amount of blood pumped by the heart, total blood volume
describe electrical activity of the heart
SA generates rhythmic AP. those electrical signal is passed to AV node
what are the mechanism through which the ANS exert control of BP
- regulation of HR
- regulation of total peripheral resistance
- regulation of stroke volume
- regulation of blood volume
how is HR regulated by the ANS
SNS mediates increase HR
PNS mediates decrease HR
how can SNS directly increase BP?
^ HR
^ total peripheral resistance
^ SV
what are baroreceptors?
- stretch receptors in the carotid sinus
- relays signal to NTS
- increase rate of firing for increase BP vice versa
how does ANS respond to increase BP? detail the players and mechanisms
- increase BP > sensed by baroR and increase FR > activates NTS > project to vagus nerve > activates PNS > release ACh onto M2 R at the SA node > M2 coupled to Gi/o > inhibit AC > - cAMP > inactivate PKA > increases outward K+ current > hyperpol > decrease HR
how does ANS respond to low BP? detail the players and the mechanisms
- decrease in BP > sensed by baroR and decrease FR > activates NTS > project to descending sympathetics (RVLM) > activates SNS > release NE onto b1 R at the SA node > couples to Gs > stimulate AC > + camp > activate PKA > decreases outward K+ current > depol > increase in HR
describe how the graph of potential vs time of the pacemaker changes in relation of activation of the ANS
the loop under the dashed line is shorter for SNS innervation > faster HR
the loop under dashed line is more like a slow trending slope for PNS innervation = slower HR
describe ANS control over total peripheral resistance (direct and indirect) + detailed mechanism
TPR can be affected by SNS but not by the PNS.
regulation of vascular smooth muscle tone is achieved through 2 mechanisms:
DIRECT: SNS postgang neurons: NE binds to a1 > Gq > PLC > IP3 > Ca2+ > binds to calmodulin > ca2+:calmodulin complex > activates MLCK > phos MLC > contraction of smooth muscle surrounding vasculature.
INDIRECT: catecholamines from adrenal medulla > epi binds a1 producing vasocon as aboved BUT also binds b2 in arterioles leading to skeletal + heart muscle > b2 > Gs > stim AC > + cAMP > PKA > inhibits MLCK > relaxation of smooth muscles (increasing blood flow to muscles and heart)
what is the net effect of SNS direct and indirect pathways
net effect is still vasoconstriction since a1 effect is overall larger.
how can stroke volume be increased
2 ways:
by increasing amount of blood delivered to the heart (more blood in more blood out) or by increasing heart muscle contractility (squeeze harder > eject more blood so less is left behind)
how does SNS regulate stroke volume
vasoconstriction of vasculature + vasodilation of arterioles leading to the heart > increase amount of blood returning to the heart (squeezing toothpaste)
SNS activation of b1 receptors > Gs > stim AC > + cAMP > PKA > + phos of Ca 2+ ch > increase ca2+ in cell from influx > increase for of contraction of cardiac myocytes
what PNS gona do about it tho
PNS can inhibit sympathetic out via inhibitory interneuron
At same time that activation of vagus nerve to activate PNS we have activation of inhibitory interneuron that inhibit descending sympathetic (indirect)
list the beta blockers (include gen, name, side effect and mechanism)
first gen: propranolol = not subtype selective (antagonist at both b1+2) side effect = bronchiole constriction
second gen: acebutolo = more selective b1 > reduce side effect
third gen: carvedilol = selective b1 over b2 and block a1
