describe how blood pressure is maintained by the arteries during ventricular contraction
- the arteries are a pressure reservoir
ventricular contraction - during the ventricular ejection phase of the cardiac cycle blood is forced into the arteries causing them to stretch
1. ventricle contracts
2. semilunar valve opens, blood ejected from ventricles flows into the arteries
3. aorta and arteries expand and store pressure in elastic walls
describe how blood pressure is maintained by the arteries during ventricular relaxation
- driving pressure for blood flow is maintained during ventricular diastole
- this is due to the elastic properties of the arteries which recoil to maintain pressure
- the energy is stored in the elastic walls
1. isovolumic ventricular relaxation
2. semilunar valve shuts preventing flow back into ventricle
3. elastic recoil of arteries sends blood forward into rest of circulatory system
what are systemic pressures (pulse pressure, MAP)
- pulse pressure = systolic pressure - diastolic pressure
-> force heart generates each time it contracts - mean arterial pressure = diastolic pressure + 1/3 pulse pressure
-> driving pressure
MAP of ____ is required to perfuse the systemic organs
- 60 mmHg
- usual range = 70-110mmHg
what is mean arterial pressure
- function of cardiac output and resistance in the arterioles
- illustrates mass balance between blood flow into the arterioles and out of the arterioles
- if arterial volume increases, pressure increases
MAP = directly proportional to CO x resistance
what are the factors that influence MAP
- increase MAP determined by
- blood volume -> increase fluid intake
-> decrease fluid loss (passive or regulated by kidneys) - effectiveness of the heart as a pump
-> increase heart rate
-> increase stroke volume - resistance of the system to blood flow
-> decrease diameter of the arterioles (increase resistance) = harder for blood to leave the arteries - relative distribution of blood between arterial and venous blood vessels
-> decrease diameter of the veins (smaller volume, so volume has to go to the arteries)
-> increase venous constriction, increase venous return, increase SV, increase MAP
how do the cardiovascular and renal systems work together to respond to an increase in blood volume
- increase blood volume = increase blood pressure
fast response
-> compensation by cardiovascular system (vasodilation and decrease CO)
= decrease pressure to normal
slow response
- compensation by kidneys
(excretion of fluid in urine, decrease blood volume)
= decrease blood pressure to normal
what are the hormones that work with the renal and cardiovascular to respond to an increase in blood volume
- atrial natriuretic peptide = atria senses high BP and releases this and causes kidney increase excretion of salt and water
- vasopressin (ADH) = if high bp less vasopressin is released
- it causes arterial constriction and conserves water
- less vasopressin = more urine and arterial dilation
what is arteriole resistance (equation)
R = Ln/r4
- resistance is equal to the length of the vessel (L) and the viscosity of blood (n) which are constant
- resistance is mostly determined by arteriolar radius
how can radius be altered
- by changes in vascular smooth muscle tone via
-> local factors - myogenic response
- paracrine
-> sympathetic nervous system regulation
explain how radius can be altered by local factors: myogenic autoregulation
- reflexive constriction of the blood vessel in response response to increased pressure
-> increase pressure (results in stretch of arteriole)
-> opens mechanically gated channels on smooth muscle membrane
-> cell depolarizes
-> opens voltage gated Ca2+ channels
-> Ca2+ into smooth muscle cell
-> increase contraction and increase arteriolar resistance
-> decreased blood flow and decrease pressure through the vessel - helps an organ maintain a constant blood flow despite changes in perfusion pressure
explain how radius can be altered by local factors: Paracrines released in response to changes in tissue needs (active hyperemia)
- active hyperemia (more blood flow) = matching flow to metabolic demand
-> increase tissue metabolism
-> metabolites released from local cells that will act on arteriole smooth muscle
-> smooth muscle cells decrease cross bridge cycling
-> vasodilation and decreased resistance
- increase blood flow to this region, thus increasing O2 and nutrient supply as long as metabolic demand is high
- metabolites = O2, CO2, H+, NO, ADP
explain how radius can be altered by local factors: Paracrines released in response to changes in tissue needs (reactive hyperemia)
- reactive hyperemia (cut off blood flow) = compensation following a period of reduced blood flow
-> decreased blood flow due to occlusion (blockage)
-> build up of metabolites (vasodilators) in ECF at this region
-> arterioles dilate, but flow still blocked
-> remove blockage
-> when blood flow is restored there is a brief period of increased blood flow due to decreased resistance
-> metabolites wash out of the region
-> arterioles regain their normal tone
what is the SNS effect on arteriole resistance
- SNS exerts tonic control on most arterioles
- norepinephrine released from postganglionic sympathetic neurons
-> binds to alpha1-adrenergic receptors on most smooth muscles
-> alpha1-adrenergic receptors are coupled to Gq (activate PLC)
-> increased IP3
-> increased Ca2+ release from SR
-> smooth muscle cell contraction
what effect does contraction increasing during exercise or stress have (NE effect on arteriole resistance)
- higher expression of alpha1-adrenergic receptors on vascular smooth muscle cells of vessels supplying skin and visceral organs (because they contract even more)
- blood flow diverted from these areas during fight or flight
explain SNS effect of NE release onto alpha1-adrenergic receptors
- arteriole diameter is controlled by tonic release of norepinephrine
- moderate signal rate results in a blood vessel of intermediate diameter
- increased NE release onto alpha receptors = signal rate increases, the blood vessel constricts
- decreased NE release onto alpha receptors = signal rate decreases, the blood vessel dilates
- diverts blood away from GI tract and sends blood to muscles
explain SNS effect of epinephrine on arteriole resistance
- epinephrine release from adrenal medulla
-> during fight or flight in response to exercise
-> primarily acts on beta2-adrenergic receptors found on smooth muscle cells of arterioles supplying skeletal muscles, heart, liver - beta2-adrenergic receptors are coupled to Gs protein -> cAMP
- cAMP causes smooth muscle relaxation
epinephrine effect on arteriole resistance of contraction
- contraction decreases during exercise or stress (radius and flow increase)
- higher expression of beta2-adrenergic receptors on vascular smooth muscle cells of vessels supplying heart, lungs and liver
-> blood diverted to these areas during fight or flight
cardiac vs smooth muscle vs vascular smooth muscle (heart, liver, skeletal muscle) (SNS effects)
- signaling moleule
- receptor
- G protein
- 2nd messenger activity
- key target protein
- effect on target proteins
- effect on muscle fiber
cardiac - NE, N -> beta1-adrenergic -> Gs-> activates AC, increase cAMP and PKA -> LTCC, SERCA -> increased activity of target proteins -> increased contractility, increase SV
smooth muscle - NE,(E) -> alpha1-adrenergic -> Gq -> activates PLC, increased IP3 -> IP3 receptor channels on SR -> increased SR Ca2+ release from IP3 channels -> increased contractility, vasoconstriction
smooth muscle (heart, liver, skeletal muscle) - E, (NE) -> beta2-adrenergic -> G2 -> activates AC, increased cAMP and PKA -> MLCK -> inhibits MLCK -> decreased contractility, vasodilation
what are baroreceptors
- pressure sensors located in walls of certain arteries
- carotid sinus and aortic arch
- nerve endings with stretch activated channels (tonically active)
- increased pressure opens more channels, more depolarization, and increase AP frequency
- reflex loop helps maintain homeostasis
-> ensures sufficient MAP for adequate blood flow to heart and brain - can affect both CO and R to change blood pressure
explain the baroreceptor reflex
- increased BP = increased firing of baroreceptors in carotid arteries and aorta
-> sensory neurons -> cardiovascular control center in medullar oblongata
= decreased sympathetic output (less NE released)
-> vasodilation of arteriolar smooth muscle (decreased peripheral resistance)
-> decreased force of contraction on ventricular myocardium (decreased CO)
= decreased BP
= increased parasympathetic output (more ACh on muscarinic receptor)
-> SA node = decreased HR
-> decreased cardiac output
= decreased BP
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