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32 Cards in this Set

  • Front
  • Back
MAP=
CO X TPR

= SV x HE x TPR
name 3 factors that can be altered to change arterial BP
1. CO (HR or SV0
2. TPR
3. BV
name 3 fast mecrhs that change BP
1. arterial baroreceptors
2. cardiopulmonary baroreceptors
3. peripheral chemoreceptors
what is the NTS
nucleus tractus solitarius

part of brainstem that receives afferent info about BP and integrates it
what is the vaso motor center
regulates efferent symp adrenergic nerve activity to peripheral resistance vessels
what regulates efferent vegal and symp andronergic activity
cardiac centers
where are arterial baroreceptors located? what do they respond to
carotid
aorta

**respond to CHANGES in stretch, these cahnges arise bc of changes in pressure
is the set point of baroreceptors permanent?
nope, the set point can be reset, ie exercise, HTN

**the baroreceptor responds to a CHANGE in stretch
how do signals from baroreceptors make it to the brain stem? what happens there? then what
vagus
glossopharyngeal n bring info from the baroreceptor to the brain

in the NTS the info is integrated


Efferent signals are then varries on vagus or SNS fibers
what do the baroreceptors do when they see increased BP
increase stretch--> take info to NTS by vagus/glossopharyngeal --> integration

**PNS is stimulated to decrease HR (SA)
**SNS is decreased, so HR decreases --> TPR decreases --> Sv decrease --> CO decreases --> MAP decreases
what do baroreceptors do when thery receive info that BP is low
increases SNS, to increase MAP
decrease PNS
what does it mean when the carotid sinus N increases its firing rate
means BP is elevated

**info from baroceceptor is carries by the carotid sinus N, which is a branch of glossopharyngeal, to the NTS. When this fires like crazy it means the baroreceptor is senseing an increase in BP
what receptors are activated when arterial P increases and the barroreceptors tell the brain
1. M2: increase to decrease HR, decrease conduction velocity, decrease contractility

2. B1: inhibited to decrease HR, decrease conduction velocity, decrease contractility

3. a1: inhibited so they dont constrict and there can be decreased TPR
how can you test the integrity of baroreceptors
Valsava Maneuver

1. expire against a closed glottis to increase intrathroacic pressure

*initial increase in MAP so HR decreases
*decrease in MAP bc venous return decreased so HR then increases
when the set point of baroreceptors is elevated due to HTN can it return to its original lower set point
sure can
where are cardiopulm baroreceptors located
low pressure areas of system: atria, veins, pulm arterires
what senses BV, cardiopolm baroreceptors or carotid
cardiopulm
what stimulates cardiopulm baroreceptors
increase in central venous volu/pressure
what happens when cardiopulm baroreceptors sense an increase in BV
1. increase HR (opposed by barpreceptors so this is hard to detect)
2. decrease vasopressin
3. renal vasodilation
4. increase in ANP
what are chemoreceptors? what are they activated by
detect changes in O2

activated by decreased O2, increased CO2, increased H+
what happens when a chemoreceptor is activated
there is decreased O2, so SNS is increased
who has a more potent resoponse, baroreceptors or chemoreceptors
baroreceptors
how does capillary fluid shoft act as a BP regulator
vasoconstriction will decrease hydrostatic p of capillaries, this decreases filtration so that more liquid is absorbed and BP is higher
when there is vasodilation of precapillary arterioles what happens to filtration/absorption. how does this affect BP
Dilation will increase hydrostatic pressure and increase filtration, this means less liquid enters the vasculature and BP is lowered
when yo have high BP the body wants to lower it so it makes sense that arterioles will...
dilate to decrease TPR as well as increase hydrostatic P of capillaries to favor filtration and have a decrease in BV bc its not being reabsorbed
name 3 things that cause renin release
1. decrease in BP
2. reduced Na flux
3. sympathetic stimulation

**increases TPR, constrictor
renin leads to dilation or constriction. how>
constriction

**renin activates angiotensin II

angiotensinogen to angiotensin I by renin
ang I to ang II by ACE in lungs
what does ANG II do?
constrictor, increase TPR
induced ADH release from adrenal cortex
what does ADH do
ANG II causes its release

**it causes Na reabs, and increase in BV
will MAP need to increase or decrease in order to have ANG II/ADH to be a good thing
decreased
when is vasopressin released?
its a constrictor

**when BV decreases, there is decreased stretch, vasopressin is stimulated to be released from post pit, increased water reabs, increased TPR, increase MAP

**LONGER TERM MEDIATOR, NO BARORECEPTOR!
vasopressin acts in what two places
vascular SM: constrictor
renal collecting tubule: increase H2O absorption