Regulation of Arterial Pressure Flashcards
TPR
effects of decreasing and increasing TPR
total peripheral resistance: determined by arterioles
a decrease in TPR causes an increase in venous return/CO
an increase in TPR will reduce venous return/CO
increasing TPR does what to arterial and venous pressure?
increases arterial pressure but decreases venous pressure
decreasing TPR does what to arterial and venous pressure
decreases arterial pressure and an increase in venous pressure
Increasing TPR effects CO or vasculature?
both: it INCREASES arterial pressure, so it must increase the afterload on the heart
Decreasing TPR effects CO or vasculature?
both: it DECREASES arterial pressure, to it decreases the afterload on the heart
Mean arterial pressure
the pressure in the major arteries delivering blood are basically the same: 100 mmHg. this pressure remains the same throughout major artery, but delivery pressure itself is controlled at the individual level by metabolic means
what is mean arterial pressure
100 mmHg
what is the formula for mean arterial pressure
P = CO x TPR
what is “deceptive” about the mean arterial pressure formula?
CO and TPR are not independent variables, so effecting one will effect the other. thus P won’t follow simple logic of an equation because it’s based on variables that alter one another.
Baroreceptors
located in carotid sinus and aortic arch
baroreceptors in the carotid sinus
respond to increases and decreases in pressure
baroreceptors in the aortic arch
respond to increases in pressure
baroreceptors are
“mechanoreceptors” which are sensitive to pressure or stretch
Which is the strongest stimulus on the baroreceptor:
Absolute pressure level
Rate of pressure changes
Changes in pressure
rate and changes
local arterial bed rely on a _____ input pressure to control how much blood the tissue receives
constant, high input pressure
Two control mechanisms for blood flow to local vascular beds
1) maintain a constant, high input pressure
2) ability to alter resistance to flow through individual vascular beds
Two general mechanisms for controlling blood flow
neuronal (baroreceptors) and hormonal
carotid sinus baroreceptors —>
herrings nerves —> CN IX
CN IX —>
+ stimulus at the Vasomotor center (medulla – nucleus tractus solitarus) —> cardiac decelerator —> (-) @ SA node
information from the aortic arch is carried by the
vagus nerve
information from the carotid sinus is carried by the
glossopharyngeal center
Vasomotor Center
how it is stimulated and what it does
baroreceptor input (increased pressure) decreases sympathetic activity and increases parasympathetic activity (decreasing heart rate)
decrease pressure –> decreased firing —> increased sympathetic activity
Increase in Pa —>
stimulation of X and IX —> vasomotor center in medulla —> increase in parasympathetics + decrease in sympathetics ———> negative stimulus of SA node + decrease sympathetic stimulation of contraction and SA —> relaxation of heart and vasodilation —> Pa brought down back to normal
Sympathetic system causes (3 things)
Parasympathetic system causes (1 thing)
constriction of arterioles and veins via alpha receptors
increases HR and contractility via beta-1 receptors
causes fluid retention by kidney due to afferent arteriolar constriction and increased renin secretion
Decrease in heart rate (muscarinic receptors)
Three centers in the Vasomotor center
Vasoconstrictor center, Cardiac accelerator center, and cardiac decelerator center
what happens when the cardiac decelerator center is positively stimulated?
it causes inhibition of SA node
Renin-Angiotensin-II-Aldosterone System
sequence leading to RENIN release
regulates Pa
decreased renal profusion —> mechanoreceptors in afferent arterioles –> decrease in Pa causes Prorenin to be converted to renin in juxtaglomerular cells
OR
beta-1 receptor stimulation on juxtaglomerular cells –> renin release
Renin-Angiotensin-II-Aldosterone System
sequence leading to Angiotensin II release
Renin converts angiotensinogen to angiotensin I
angiotensinogen
angiotensin II in the heart and lungs specifically
catalyzed from angiotensin I by angiotensin converting enzyme (ACE) in the heart and lungs
increase blood volume, preload, stroke volume, CO and therefore BP
Angiotensin II
apart from heart and kidneys, where does this protein work?
vascular smooth muscle, brain, and adrenal cortex
it stimulates G coupled protein-couple angiotensin II receptors (ATi)
i
Angiotensin II —> aldosterone
increases aldosterone, which increases sodium reabsorption
kidneys
Angiotensin II –> Na-H exhcnager
increases their activity in the kidneys, stimulating sodium reabsorption
Angiotensin II –> hypothalamus
increases thirst and release antidiuretic hormone
Angiotensin II —> arterioles
increase TPR —> increasing arterial pressure
achieves this by binding to g coupled protein receptors and causing an upswing of cAMP–>IP3–>DAG—>Ca2+
big picture theme of Pa’s relationship to angiotensin II
as Pa decreases, angiotensin II tries to restore it
why is the baroreceptor induced over the hormone method of restoring Pa, and vice versa?
baroreceptors can work in seconds but are considered long term and short term mechanisms
hormones are needed for long term pressure maintenance
from Ballam slides
angiotensin I is converted by ____ in the _____. (1)
angiotensin I is converted to ____ in the _____ as well (2)
angiotensin converting enzyme in the blood and in the kidneys as well
“ultimate relationships”
angiotensin II —> aldosterone —>……
angiotensin II —> aldosterone from adrenal cotex —> Na-H pump in the kidneys —> Na retention —> water reuptake —> Pa —> increased preload –>increased SV –> increased CO –> increased BP
ADH
released by hypothalamus in response to angiotensin II
binds to receptors on arterioles and causes vasoconstriction (increasing TPR)
binds to kidney cells and stimulate reabsorption
remember:
angiotensin II —> site of action —> increased blood volume –> increased preload —> increased SV —> increased CO —> increased BP –> increased Pa
vasopressin
ADH
side effect of ACE inhibitors
angiotensin converting enzyme convers angiotensin I to II, but it also breaks down bradykinin which accumulates and can make you cough
ARBs
angiotensin receptor blockers
cerebral ischemia
causes increased sympathetic outflow from vasomotor center
Hemorrhage cause blood to
drop
means loss of blood volume
Hemorrhage causes what parts of the vasomotor to work, and how
decreased blood volume —> decreased stretch on baroreceptors at carotid sinus –> decreases signals to brain–> induce sympathetics in heart —> heart rate/contractility increase —> decreases unstressed volume
Valsalva maneuver
expiring against a closed glottis
causes increase in intrathoracic pressure
decreases venous return
Cushing reflex
as intracranial pressure increases, cerebral arteries are compressed –> decreased perfusion in the brain
CO2 and therefore H is not removed from the brain, so the pH drops, which causes medullary chemoreceptors to cause sympathetic outflow toward brain
in a nuttshell: intracranial pressure redues blood flow to medulla, activating sympathetics to increase outflow to brain. over all effect is increase in TPR and Pr
Vasopressin is released
in response to angiotensin II from brain
also released by r. atria in response to low preload
causes increased TPR and water retention
Natriuretic peptide :ABC
Atrial, Brain, C-type
causes arteriolar dilation, increases fluid loss
inhibits renin
decrease TPR at atrioles
secreted by excessive preload of atria and ventricles
