Central Neural and Humoral Control of Blood pressure Flashcards
What is the over all effect of the sympathetic N.S. on TPR?
Increases
Vasoconstrictor sympathetic fibers are widely dispersed, where are they most/least concentrated?
Most: Kidney and skin
Least: heart and brain
•Norepinephrine:
Adrenoceptors on VSMC -> generalized vasoconstriction (pressor effect)
The exceptions include?
•Exceptions include skeletal and cardiac m. response can promote vasodilation (β2 )
What is the primary neural influence on arteriolar smooth muscle?
Via what receptors and NT’s is this accomplished?
Sympathetic
Vasoconstriction:
α₁ receptors: Norepinephrine, epinephrine
Vasodilation
β₂ receptors preferentially bind epinephrine (expression: skeletal m., cardiac m., liver, & adrenal medulla
What are the five components of the negative feedback loop involved in neural reflexes?
- Receptor
- Afferent path
- integration center
- efferent path
- effector
What are the receptors involved in MAP regulation?
Baroreceptors
Chemoreceptors
What types of baroreceptors are there? What do they detect?
mechanoreceptors, detect stretch
–High-pressure receptors
–Low-pressure receptors
What do chemoreceptors detect?
detect changes in blood PO2, Pco2, [H+]
What is the primary integration center involved in MAP regulation?
medulla oblongata; cerebral cortex & hypothalamus
What are the 4 effectors of MAP regulation?
–Cardiac myocytes (pacemaker & contractile)
–Arterial & venous vascular smooth muscle cells (VSMCs)
–Adrenal medulla
–Kidneys
What six things provide feedback to the medulla oblongata?
–Baroreceptors
–Chemoreceptors
–Hypothalamus
–Cerebral cortex
–Skin
–Local CO2 and O2 concentrations
What are the most important high-pressure baroreceptors?
Carotid sinus and aortic arch
What does an increased receptor stretch due to increased pressure lead to regarding high pressure receptor firing rate?
Increases it.
(graded response with amplitude proportional to amount of stretch)
Outline the 8 steps of the high-pressure baroreceptor reflex response to increased MAP.
(Important)
Baroreceptors respond to increased MAP by causing vasodilation and decreased heart rate. Describe how this is accomplished beginning with the stretch sensation
TPR
–↑ Baroreceptor stretch
–↑ Baroreceptor firing rate
–Inhibition of vasomotor area
–↓ Sympathetic output
–↓ vasoconstriction
–↑ Vasodilation
HR
–↑ Baroreceptor stretch
–↑ Baroreceptor firing rate
–Excitation of interneurons in cardioinhibitory area
–↑ Parasympathetic output
–↓ Heart Rate
Which baroreceptors predominate?
What kind of pressure to these mostly respond to?
- Carotid baroreceptors predominate over aortic
- Greater response to pulsatile vs. steady pressure
What are the low-pressure baroreceptors? Where are they found? What do they regulate?
Cardiopulmonary receptors:
- In cardiac chambers and large pulmonary vessels
- Involved in blood volume regulation
What do the A and B fibers of the low pressure baroreceptors monitor respectively?
•A fibers: monitor HR (fire during atrial systole)
B fibers: monitor atrial volume
What is the response of increased low pressure baroreceptor firing rate? (on heart rate and renal vessels)
Reflex Response:
•↑ HR•↓ Renal vasoconstriction
(Promotes renal vasodilation)
–↑ Renal blood flow
–↑ Urine output
–↓ Effective circulating volume
What does the bainbridge reflex do?
Counterbalances the high-pressure baroreceptor reflex
- ↑stretch of high-pressure receptors → ↓ HR
- ↑stretch of low-pressure receptors → ↑ HR
- High-pressure baroreceptors: generalized vasodilation
- Low-pressure baroreceptors: renal vasodilation
At what point in the cardiac cycle is the bainbridge reflex dominant?
During volume loading
During which point of the cardiac cycle is the high pressure baroreceptor reflex dominant?
volume depletion
At low blood volume, what impact does the baroreceptor reflex have on the slope of the starling relationship?
•Baroreceptor reflex
↑ sympathetic output ->↑ contractility & slope of Starling relationship
At high blood volume what impact does the baroreceptor reflex have on the starling relationship?
•↓ sympathetic output -> ↓ contractility & plateau of Starling relationship
What are the peripheral chemoreceptors? Where are they located?
•Carotid body (carotid a. bifurcation)
Aortic bodies (aortic arch)
What do peripheral chemoreceptors do?
Detect changes in arterial blood
What does the chemoreceptor reflex do?
–Primarily regulates respiration
(increased rate and depth)
–Some influence on cardiovascular system
(vascular tone and HR)
What is the chemoreceptor integrated physiologic response?
Vasoconstriction and tachycardia
If ↓ MAP and ↑ Pco2 ↓ pH ↑ [H+] occur simultaneously, what happens?
•↑ stimulation of chemoreceptors and ↓ stimulation of baroreceptors -> ↑ vasoconstriction
If ↑ Pco2 ↓ pH ↑ [H+] occurs along with ↑ MAP
•↑ stimulation of chemoreceptors and ↑ stimulation of baroreceptors -> (ex: high carotid sinus pressure and low Pao2) -> baroreceptor-mediated inhibition of vasoconstriction dominates
What are the major hormones that control vascular resistance?
4
- Epinephrine
- Angiotensin II (ANG II)- Atrial natriuretic peptide (ANP)
- Anti-diuretic hormone (ADH) = Arginine Vasopressin (AVP, Vasopressin)
What are the hormones that control blood volume?
3
Anti-diuretic hormone (ADH) = Arginine Vasopressin (AVP, Vasopressin)
- Aldosterone
- Atrial natriuretic peptide (ANP)
What hormone controls heart rate and stroke volume?
Epinephrine
Where is epinephrine produced? What does it do when binding alpha 1 and beta 2 receptors respectively?
adrenal gland
- Vasoconstriction via α₁, vasodilation via β₂ receptors
What is ANG I converted to ANG II by? What does it do? What is it stimulated by? Where is it released?
Converted from ANG I by ACE (mainly in lungs; ACE is secreted by pulmonary and renal endothelial cells)
- Vasoconstriction
- Ex: released during blood loss or exercise
- ↓renal BP à stimulates renin release
What is the effect of ADH/AVP that is released by the posterior pituitary? When is it released?
Vasoconstriction
- Ex: released during hemorrhagic shock
Histamine is released in response to tissue trauma, what is the result of this?
Vasodilation (arteriolar), Venoconstriction
Atrial myocytes release ANP, what does this lead to?
Vasodilation
Characterize the response time of endocrine control of blood volume
Long-term
What is the key effector organ for long term blood volume regulation? How does it regulate this?
Kidney
–Regulation of Na+ and H2O excretion in urine
What are the 3 humoral regulators of blood pressure?
- Renin Angiotensin Aldosterone System (RAAS)
- Antidiuretic Hormone (ADH)/Vasopressin (AVP)
- Atrial Natriuretic Hormone (ANH/ANP)
Review the renin-angiotensin-aldosterone system on slide 70. Draw it.
What are the major effects of angiotensin II? (6)
- Vasoconstriction
- Stimulates adrenal gland aldosterone production
- Stimulates ADH/AVP
- Stimulates thirst
- Stimulates renal Na+ reabsorption
- Stimulates SNS activity
What triggers secretion of aldosterone by the adrenal cortex? What does it promote?
What does this do to MAP?
ANG II
- Promotes renal Na+ reabsorption
- H2O follows by osmosis
- ↑ Effective Circulating Volume•↑ MAP
If the hypothalamus detects increased osmolarity, what does it do?
Stimulate fluid retention by increased release of vasopressin (and ANGII) by the posterior pituitary gland. Leads to increased MAP
What system does the atrial natriuretic peptide/hormone oppose?
renin-angiotensin-aldosterone system
•Cardiac atrial cells (low-pressure baroreceptors) detect: ↑ wall stretch (↑ blood volume), what do they do in response?
What is the impact on MAP?
- Secrete ANP (vasodilator AND natriuretic)
- Results in ↓ renal Na+ reabsorption↑ Na+ excretion = natriuresis↑ H2O follows in urine
•↓ ECF volume, ↓ ECV, ↓ MAP
Identify the neural and hormonal responses shown in the graph
Understand the integrated response to a decreased effective circulating volume/MAP
Slide 80
What is the dominant reflex responding to orthostatic changes?
What is the ANS response?
This leads to what regarding the muscle pump?
High pressure baroreceptor reflex responding to volume depletion.
•↑ Sympathetic; ↓ parasympathetic
Increased muscle pumping for increased venous return
What is the vasovagal (vasopressor) syncope a common response to?
•sudden emotional stress, acute pain, sight of blood, etc.
The vasovagal syncope response follows this pathway:
•(Vagal afferents) -> Higher CNS -> medulla oblongata:
–Dramatic ↑ parasympathetic output
– ↓ sympathetic output
What physiological changes result from this path?
•Bradycardia and hypotension
–↓ TPR, ↓ CO, ↓ MAP
Loss of consciousness: ↓ cerebral perfusion pressure
In vasovagal syncope MAP decreases due to diminished TPR and CO, due to failure of activation of what response?
Baroreceptor Response
What are the peripheral receptors and reflexes involved in the fight or flight response?
No peripheral receptors or reflexes
How is blood flow to skeletal muscle increased in response to the fight or flight response?
•Adrenal medulla: epinephrine
–β2 adrenoceptor activation
–Vasodilation and ↑blood flow: skeletal m.
–If exercising: metabolite production also promotes vasodilation and ↑ flow via autoregulation
During fight/flight, there is general vaso- and venoconstriction, how is this accomplished?
•Sympathetic output: norepinephrine & epinephrine
–α1 adrenoceptor activation
–↓ Renal and Splanchnic blood flow
During F/F response how is cardiac output increased?
–↑ sympathetic and ↓ parasympathetic output
–↑ HR and ↑ SV (↑ contractility)
During F/F response, how is blood volume maintained?
–↑ ADH/AVP -> ↓ urine output
In F/F what causes the net increase in MAP?
–↑ CO
–Increase/decrease in TPR
•Depends on balance between vasodilation and vasoconstriction
What are the central command changes in response to exercise?
How about local responses?
(Important)
Slide 95
What organizes the early neural response in ANTICIPATION of exercise?
Hypothalamus
What are the delayed responses to exercise?
•Mechanical response:
–Muscle pump
–Increased VR
•Chemical response:
–Autoregulation of exercising skeletal m.
–Metabolites -> vasodilation
–↓ TPR
During exercise, what do muscle afferents and reflexes reinforce?
Sympathetic output
What is the impact of exercising muscle on capillary hydrostatic pressure?
•Increased capillary hydrostatic pressure
–Arteriolar dilation
–Net fluid filtration
–↑ interstitial fluid hydrostatic pressure
•↑ lymphatic flow
What is the increased O2 delivery during exercise due to?
•oxyhemoglobin dissociation relationship
–↓ pH
•Due to ↑ CO2 and lactic acid
–↑ temperature
–↓ Hb affinity for O2 , promotes “off-loading”
By what factor can O2 consumption increase during exercise?
60x
What are the 6 components of the integrated CV response during exercise?
- Exercise pressor reflex
- Sensitivity of baroreflexes
- Skeletal m. vasodilation
- Circulating epinephrine
- Venous return
- Temperature regulation
Where does the exercise pressor reflex originate? What receptors mediate?
–Reflex originates within the exercising muscle -> Neural drive
•Stretch receptors: muscle tension
•Chemoreceptors: metabolites
During exercise, we have continued sympathetic output despite increased MAP. How is this possible?
Arterial baroreflexes
–Re-set of arterial baroreflex sensitivity by central command
Metabolites released locally dilate resistance vessels during exercise, to what degree is this possible?
20x
Venous return increases during exercise, what causes this? What factors contribute to this balance?
–Muscle pump: ↑ VR à ↑ SV (Starling’s law) à ↑ CO
–Balance of SV, HR, Contractility, Relaxation rate
What fibers maintain temperature regulation during exercise? How do they do it?
–Sympathetic cholinergic fibers activate to sweat glands
–Inhibition of sympathetic vasoconstriction to skin (constricted in early response) à↑ cutaneous flow
How is stroke volume maintained in exercise induced tachycardia?
What is the major cardiovascular component that decreases with exercise? What does this serve to offset?
MAP: General Increase
SBP > DBP
↑ PP
- Due to increased CO
- Offset by overall decrease in TPR
