Lec 13 Regulation of BP Flashcards
How can we rearrange Ohms low for physiology?
MAP = CO * TPR MAP = mean arterial pressure CO = cardiac output TPR = total peripheral resistance
What does an increase in MAP do to CO?
nothing! – it is a one way causal relationship
What does increase in CO do to MAP?
increase in CO causes increase in MAP
What does increase in TPR do to MAP?
increase in TPR causes increase in MAP
What is equation for MAP [from DP and SP]?
MAP = 2/3 DP + 1/3 SP
because diastole lasts longer than systole
does systole or diastole last longer?
diastole twice as long as SP at rest
Where are baroreceptors? Function?
- located in carotid sinus [mostly] and aortic arch
- initiate rapid response to changes in BP
What is function of atrial volume receptors?
- respond by releasing ANP
Where are chemoreceptors? what do they respond to?
- in carotid bodies and aortic arch
- respond to changes in O2 levels
What is function of mechanoreceptors in kidney afferent arterioles?
- activate RAAS
In what conditions do baroreceptors send impulses to medulla?
- more impulses at higher pressure, fewer impulses at decreased pressure
3 phases of baroreceptor response?
- change in MAP, this is direct response before any reflexes engaged
- reflex response tries to change MAP to normal
- after changes by reflex, new steady state is reached
pathway of response to acute decreased MAP [ex in hemorrhage]
- decreased blood volume –> decreased preload –> decreased stroke volume –> decreased CO –> decreased MAP
What happens to SV at higher LVEDP [left ventricular end diastolic pressure]?
- higher LVEDP = more fill, get more ejection of fluid but also a higher percentage of fluid ejected / higher contraction
Do you get more impulses from baroreceptors to medulla at increased or decreased pressure?
at increased pressure
What are effects of reduced baroreceptor firing?
- increase S to SA –> increase HR
- decreased PS to SA –> increase HR
- increased S to ventricles –> increase contractility
- increased S to arterioles –> increased TPR
- increased S to veins –> venoconstriction
What are the 2 molecular mechanisms of the reflex response on HR to low MAP?
- decreased PS –> decreased activation of IkAch by By subunits
- increased S –> increased activation funny current by cAMP
What 4 drugs mimic effect of baroreceptor reflex to low MAP [on HR]? What do they do to HR?
Atropine: inhibits PS
Isoproterenol: B agonist
Norep/Epi
increase HR
What is effect on contractility of reflex response to MAP?
increased sympathetic output to ventricles –> increased cellular contractility –> higher SV for same ventricular filling
- more B stimulation, more camp, more PKA –> phosphorylation L-type Ca channels and phospholamban
What 3 drugs mimic effect of baroreceptor reflex on low MAP [on contractility]? What do they do?
- NE, epi, isoproterenol
- increase contractility, faster relaxation, bigger stroke volume
What is reflex response on TPR in low MAP? Mech/path?
- more sympathetic output to arteriole smooth muscle cells –> more TPR
- get more a1 stimulation –> release of Gq a subunit –> activates phospholipase C –> produces IP3 –> SR Ca release [slow compared to RyRs] –> contraction
- smooth muscle contraction –> increased vessel resistance due to contraction [smaller radius]
Drugs that mimic reflex response on TPR in low MAP?
acts via a1
NE
phenylephrine [a1 agonist]
Drugs that inhibit reflex response on TPR in low MAP?
phentolamine [a1 blocker]
What is reflex response on venoconstriction in low MAP? what effect does this have?
- increased sympathetic output to veins causes venoconstriction [via a adrenergic stimulation]
- -> causes reduced venous compliance –> fluid can’t stay stored in veins so goes back to heart –> get increased ventricular filling / preload
2 effects of baroreceptor reflex [in low MAP] on myocardium?
- increased HR [SA] –> increases CO
- increased contractility [ventricle] –> increases CO
2 effects of baroreceptor reflex [in low MAP] on vessels?
- arteriolar smooth muscle contraction –> increases TPR
- venous smooth muscle contraction –> increases preload –> increases CO
Do changes in contractility affect systolic or diastolic?
systolic
Do changes in arterial pressure affect systolic or diastolic?
diastolic
When are atrial stretch receptors activated? What do they do?
in high blood volume they cause atria to release ANP into bloodstream
What does ANP do [2 things]?
- vasodilate blood vessels –> lower TPR –> lower MAP
- block renal Na reabsorption –> increase Na excretion –> lower blood volume
In what circumstance does the heart act as an endocrine organ?
when atrial stretch receptors activated and release ANP into bloodstream
What is function of central chemoreceptors?
- in carotid bodies and aorta
- response to decrease in blood O2
- cause vasoconstriction and changes in breathing
What is effect of chemoreceptors on vessels?
- low O2 –> chemoreceptors signal to increase S to arterioles –> increased resistance
- causes vasoconstriction in renal, skeletal muscle, splanchnic [GI] circulations
How is blood pressure regulated long term?
renin-angiotensin-aldosterone system [RAAS]
What is pathway of RAAS?
- decreased pressure in kidney causes release renin from juxtaglomerular cells
- increased renin –> increased angiotensin II
- increased angiotensin II which:
——> increased aldosterone –> increased Na reabsorption in kidney –> increased blood volume
——> direct vasoconstriction –> increased TPR
Where is renin released from? in response to what?
- released from juxtaglomerular cells in kidney
- in response to decreased pressure in kidney
2 steps of angiotensin II release? What enzymes?
Renin: activates angiotensinogen –> angiotensin I
angiotensin converting enzyme [ACE]: activates angiotensin I –> angiotensin II
What are 2 direct effects of angiotensin II?
- increases aldosterone
2. vasoconstriction [via increased release of Ca leading to smooth muscle contraction]
What is effect of aldosterone?
increases Na reabsorption in kidney –> increases blood volume
What are 2 effects/pathways induced by angiotensin II?
——> increased aldosterone –> increased Na reabsorption in kidney –> increased blood volume
——> activates release of Ca in vascular smooth muscle–> contraction –> vasoconstriction –> increased TPR/BP
What is long term effect of angiotensin II?
- Angiotensin II can reset baroreceptor response
- shift curve so have higher HR for a given BP, this keeps BP/MAP up
What time fram for baroreceptor vs atrial stretch receptors vs RAAS vs chemoreceptors?
baroreceptor reflex = short term change MAP
atrial stretch = medium term change MAP
chemoreceptor = mild change MAP, altered breathing
RAAS = long term change MAP
