Regulation of BP - Dr. Rogers Flashcards
CASE 1 38yo infusion of isotonic saline solution for a hangover, and too much was added
What sensed the addition of blood volume in the body
BARORECEPTORS (FAST)
Slow ways of regulating BP
RAAS (renin-angiotensin- aldosterone- system
ADH and ANP
Equation for MAP
MAP = CO x TPR MAP = HR x SV x TPR
Baroreceptor pathway
- BARORECEPTORS on the TPR channels sense stretch of Artery wall
- Increase firing of afferent n
- Signal to medulla
- Para and sympa go to cerebral cortex and hypothalamus (efferent n)
- Change MAP (by changing CO or TPR)*
Where are the BARORECEPTORS found and what nerve is there sending the signal
- Carotid sinus : (CN9) +sinus n of Hering
- Aortic Sinus : CN10 + Aortic nerve
= BOTH go to Nucleus Tractus Solitarius and release GLUTAMATE
Chemoreceptors respond to what
Po2 and Pco2 and pH
Low firing of CN 10 and CN9 to NTS causes end goal of
Increase BP
BARORECEPTORS respond to magnitude of or rate of change in BP
RATE of change of BP (fast change in pressure activates them)
Which BARORECEPTORS has highest threshold
Also normal range for picking up BP
Aortic sinus
40-60mmHg to 200mmHg
Parasympathetic function on heart
HR ( to SA node muscarinic R) * only CO (not TPR)
NOT contractility
After signal to NTS where does signal go
- To Vagus nucleus or nucleus ambiguus———> send PARAsympathetic to SA and AV node (cardioinhibitory area)
- To Ventrolateral medulla ——> SYMPAtheic to heart (A, V, SA) + arteries + veins
Sympathetic function on low BP
3 ways
- A receptors: constriction of arteries and veins (TPR)
- B1 receptors: increase HR and contractility (CO)
- Kidney fluid retention : constriction afferent arteriole + release renin
Orthostatic HTN
Lying down and standing up causes:
- lightheaded, dizzy, normal movement helps move blood back to heart
Reason Orthostatic HTN happens
- Lying down causes blood to pool in legs(can cause edema)
- VR and CO decrease
- MAP decrease
- BARORECEPTORS activated
- Increase sympathetic outflow
- Something doesn’t happen : TPR increase, increase HR, contractility, CO, vein constriction, VR, decrease in unstressed volume
- BP doesn’t go back to normal right away *ANS dysfunction
BARORECEPTORS in HTN patients
They adjust to the new normal (reason its not active in HTN pts)
RAAS system steps
Over time regulation of right BP for the body
- Liver secretes Angiotensinogen
- RENIN (from juxtaglomerular cells) converts it to angiotensin 1
- ACE (from kidney and lungs) converts it to angiotensin 2
- Angiotensin 2 acts to increase BP
Angiotensin 2 functions
- Kidney. Contract glomerular efferent arteriole
- PP : secrete ADH (increase H2O reabsorption)
- Vascular SM : HTN
- Hypothalamus: thirst
- Adrenal cortex : Aldosterone (increase NA+ reabsorption)
2 things that cause Renin to be secreted
- Nerve to B1- receptor (sympathetic)
2. low NaCl at macula densa
Where are juxtaglomerular cells found
On afferent arterioles
How does angiotensin 2 cause vasoconstriction
Binds to AT1 receptors on vessels to increase TPR and BP
BP equation
BP = CO x TPR
Increase Blood volume causes what preload SV CO BP
All increase
Where does ADH bind
function
V5 receptors (SM) V2 receptors (Collecting Ducts) * increase H2O reabsorption + increase TPR (vasoconstriction)
4 things making ADH secretion
- Angiotensin 2
- Low preload (atrial receptors
- Increased osmolarity in blood (viscosity)
- Sympathetic NS
Natriuretic Peptides (there are 3)
ANP (atrial)
BNP (brain)
CNP (C-type)
Natriuretic Peptides function
- Dilation of arterioles
- Decrease preload (increase fluid loss)-> lower ADH and aldosterone
- Inhibit renin (decrease TPR and preload
* protect against overstretch of cardiac chambers
What released Natriuretic Peptides
Excessive PRELOAD or A or V = releases ANP
How long can BARORECEPTORS keep up with blood loss without permanent damage where ADH and RAAS can’t bring back BP to normal over time
2 hours
American Heart association recommends how much salt intake
No more then 2,300mg a day
Ideal 1,500mg / day
Try to cut to 1,000mg / day
Increased Na+ in blood can cause what to ANS
Increased Sympathetic NS and increased TPR
What is heart failure
Reduced CO and SV
*ventricular dysfunction
What happens in heart failure to BP regulation systems
RAAS and Sympathetic NS increases
ANP/BNP increased also
What happens during exercise
- Increased sympathetic NS
- Decreases parasympathetic
- Increased HR + contractility + VR + vasoconstriction in some areas
- Vasodilation to SM = Overall decrease in TPR*
- SBP increase, DBP no change
