Regulation of BP Flashcards
(36 cards)
SNS and MAP
increases TPR, HR, SV
therefore increases MAP via vasoconstriction
also causes release of Epi from adrenal medulla which amplifies the effects of NE
SNS and TPR
increases TPR through vasoconstriction (pressor effect) NE/Epi—>VC in smooth muscles
-exceptions include skeletal and cardiac m (Epi—>B2—>VD)
Exercising vs. resting skeletal muscle and SNS
Resting skeletal muscle: neural control dominates—>VC
exercising: intrinsic regulation dominates—>VD
* *local metabolic effect overrides SNS output
PSNS and MAP
indirect (think NO) promotion of VD—>decreased TPR (minimal effect due to lack of receptors)
decreases HR
Decreases contractility
*decreases MAP
Medulla Oblongata
- *Major CV integrating center: vasomotor area
- regulates MAP
- mediates SNS and PSNS outputs
Input to MO
Baroreceptors, chemoreceptors, cortex, skin, local Co2 and O2
High pressure baroreceptors
Located at aortic arch and carotid sinus
inc MAP—>inc stretch—>inc receptor depol—>decrease SNS—>VD and bradycardia
rate(graded upon degree of stretch)
-respond to change in pressure:respond more to increased pulse pressure-not mean pressure
Increased MAP on high pressure Baroreceptors
inhibition of vasomotor area—>dec SNS–>dec VC—>VD
Impact of inc HR on baroreceptors
excitation of interneurons in cardioinhibitory area—>increases PSNS output—> dec HR
Low pressure baroreceptors
located in cardiac chambers (RA) and large pulmonary vessels (IVC) (in low pressure regions)
inc filling pressure/stretch—>increase FR
—>monitor blood volume (atrial filling) —> inc HR and dec renal VC–>inc urine output—>decreased effective circulating volume
Brainbridge reflex
increase VR/RAP–>inc HR (want to move extra blood volume through more quickly)
wins out over HPB response during times of high volume
counterbalance High pressure baros (which slow HR to compensate high pressure)
SV and HPB
–>inc MAP—>activates HPB—>decrease SNS—>dec contractility and flattening (plateau) of starling releationship
SV and LBP
activates LBP—>inc SNS output—>increase contractility and slope of Starling curve
Peripheral chemoreceptors
located at the carotid bodies or aortic arch near HPB
**detect inc CO2 and dec pH (some dec O2
increase rate and depth of respiration, some influence of vascular tone, and HR
Central chemoreceptors
in the MO
detect changes in central CO and decreased pH (indirect)
inc CO2—>stim vasomotor area—>VC—>increased TPR (in hopes of increasing MAP which maintains adequate driving force to supply the brain)
Net effect of chemoreceptor activation
inc HR, inc TPR, inc MAP (thru inc SNS)
Baroreceptor vs Chemoreceptor response
if there is a increase pCO2 and increase in MAP, both would be stimulated, but baro-mediated inhibition of VC wins out
Epinephrine
from adrenal gland
VC (a1)
VD (B2)
ANG II
converted from ANG I by ACE (lungs)
VC (from renin in Kidneys during blood loss and exercise )
ADH/AVP
from posterior pituitary gland
—>VC, released during hemorrhagic shock
Histamine
response to tissue trauma
Vasodilation and Venoconstriction
ANP
from atrial myocytes (LPB receptors)—>VD
**causes increase Na excretion (H20 follows)
opposes ADH in RAS system in order to decrease MAP
long term regulation of BP
done by non-vasoactive factors thru regulation of blood volume
**kidney is key
RAAS
main function is to maintain Na reabsorption —>increase MAP
occur in response to dec blood volume
