Regulation of Blood Pressure

Question 1

What is the eqn for MAP?

Answer 1

(SBP +2*DBP)/3 or pulse pressure/3 + DBP

Question 2

What is pulse pressure?

Answer 2

SBP-DBP

Question 3

Is pulse pressure higher in muscular arteries (e.g femoral artery) downstream of ascending aorta or in the ascending aorta itself?

Answer 3

downstream, due to decreased compliance as compared to aorta (an elastic artery).

Question 4

If pulse pressure is higher downstream of the ascending aorta, how can blood flow?

Answer 4

MAP in the femoral artery is lower than in aorta, thus allowing blood to flow from aorta to peripheral arteries, via Ohm’s Law.

Question 5

Why does pulse pressure increase in the aorta with increasing age?

Answer 5

The aorta becomes less compliant, although this does not significantly change MAP

Question 6

What are the main systems that regulate arterial pressure?

Answer 6

1) rapidly responding systems (5 sec to 1 min)2) Less rapidly responding systems (1-30 min)3) Slowly responding systems (days to months)

Question 7

What is the main effect of rapidly responding systems?

Answer 7

these systems are designed to buffer changes in pressure, not set new ones

Question 8

What players are involved in rapid response to AP?

Answer 8

• baroreceptors- chemoreceptors- regulation of SV by atrial pressure (after load)- cerebral ischemia-induced response

Question 9

What nerves are involved in baroreceptor regulation of arterial BP?

Answer 9

baroreceptors on the aortic arch connect to the vagus nerve which transmits to the brain, and Hering’s nerve from the carotid sinus near the bifurcation of the internal and external carotids connect to the glossopharyngeal nerve to the brain

Question 10

The baroreceptor is aka?

Answer 10

carotid sinus

Question 11

The chemoreceptor is aka?

Answer 11

carotid body

Question 12

Once increased arterial pressure is sensed by baroreceptors, where does it transmit?

Answer 12

the effector is the nucleus tractus solitarius in the medulla of the brain as well as the cardiovascular system

Question 13

What does the nucleus tracts solitarius do in response?

Answer 13

The response of the effector to information that indicates increased arterial pressure is to decrease sympathetic and increase parasympathetic activity.

Question 14

What is feedback gain?

Answer 14

the strength of the feedback employed by the nucleus tracts solitarius.

Question 15

Describe feedback gain.

Answer 15

let’s suppose that there is a 10 mm Hg increase in arterial pressure. After the system is allowed to operate, the 10 mm increase is reduced by 5 mm. Thus, the correction is 5 mm and the “error” (amount that could not be corrected) is also 5 mm, giving a gain of 1 (5 divided by 5). Had the 10 mm increase been reduced to 1 mm, then the correction would have been 9 mm and the error 1 mm and the gain 9. Thus, it is possible to calculate the gain or “strength” of the homeostatic feedback system. This is important to allow a comparison of different mechanisms that are involved in regulation of blood pressure.

Question 16

What information do baroreceptors convey to the CNS?

Answer 16

-MAP-pulse pressure-HR

Question 17

How is info about MAP conveyed?

Answer 17

action potentials that increase in quantity with rising MAP convey the signal

Question 18

Describe the relationship between isolated carotid sinus pressure (x) and systemic arterial pressure (y).

Answer 18

reverse sigmoid shape As we decrease the pressure on the sinus from the set point (the sensed “normal” pressure), the baroreceptor system responds by increasing systemic arterial pressure. This is effected by increasing sympathetic activity and decreasing parasympathetic activity. As a result, inotropy (cardiac contractility) and chronotropy (heart rate) both increase, causing an increase of cardiac output. Simultaneously, veins constrict and become less compliant, further increasing cardiac output via effects on the vascular function curve. Finally, resistance arterioles constrict under the influence of increased sympathetic activity, increasing TPR. These events, taken together, increase blood pressure to compensate for the “sensed” decrease of pressure at the carotid baroreceptor. It is also important to note that the steepest portion of the curve is at the set point, that is the sensitivity of the system is greatest when defending against deviations from the arterial pressure defined as “normal”. Also important to note is the fact that the baroreceptors can buffer against both increases and decreases of blood pressure.

Question 19

Pulse pressure also regulates arterial pressure via the baroreceptor system independent of MAP. How?

Answer 19

the higher the pulse pressure, the lower the systemic arterial pressure, indicating that the baroreceptor system responds to pulse pressure.

Question 20

The baroreceptor system also responds to the rate of pulses i.e. the heart rate, independently of other variables. How?

Answer 20

The number of nerve action potentials is integrated over time and the greater the number of action potentials (the greater the heart rate), the more the NTS will tend to reduce sympathetic activity and increase parasympathetic activity and vice versa for decreased pulse rate.

Question 21

How do we know that baroreceptors don’t set pressures, only buffer them?

Answer 21

When a dog’s carotid sinus was denervated, the following happened:1) the mean arterial pressure remained the same 2) the variability of blood pressure was much greater than in the normal dog with intact baroreceptor activity.

Question 22

Baroreceptor monitoring is an acute mechanism of regulating BP. How do we know this?

Answer 22

Almost immediately following increased BP, the baroreceptor system will take measures to oppose this increase, by decreasing sympathetic and increasing parasympathetic activities such that within minutes, most of the increase has been able to be reversed. However, after a day or so, the pressure returns to the high value if the cause persists. This indicates that the baroreceptor plays no long term role in setting the value of blood pressure and that it “resets” or “adapts” to chronically altered pressures.

Question 23

Baroreceptors exist in both carotid and aortic forms. Which one is more effective?

Answer 23

carotid- can buffer BP ranging from 50-200 mm Hgaortic- can buffer BP ranging from ~70-200 mm Hgbut a take-home is that they are both very effective in the short term and can buffer decreases and increases in BP

Question 24

Reduction of MAP below ___ activates chemoreceptors.

Answer 24

80 mm Hg. Thus, chemoreceptors only function to buffer severe HYPOtension

Question 25

What are chemoreceptors sensitive to?

Answer 25

low oxygen and/or high CO2 levels

Question 26

T or F. Unlike baroreceptors, activation of chemoreceptors stimulates sympathetic and parasympathetic activity together

Answer 26

T. However, the effect of sympathetic activation overrides the effect of parasympathetic activation, causing an overall increase of AP

Question 27

Describe cerebral ischemia-induced response to AP changes.

Answer 27

Reduction of arterial pressure below 60 mm Hg activates an intense sympathetic and parasympathetic discharge with the effects of sympathetic activation prevailing. The is a last-ditch response to maintain blood flow to the brain

Question 28

T or F. Cerebral ischemia-induced response responds to HYPOtension only

Answer 28

T.

Question 29

What is the Cushing reaction?

Answer 29

(aka Cushing reflex) is conceptually related to the cerebral ischemia response and occurs because of increased intracranial pressure, compressing cerebral resistance arteries. This can be demonstrated in a dog experiment by artificially increasing intracranial pressure which then results in increased arterial pressure. The increase of arterial pressure counteracts decreased blood flow induced by increased intracranial pressure. The Cushing reaction can occur in patients in which the intracranial pressure is increased and would present as HTN combined with bradycardia

Question 30

What are some systems that regulate arterial pressure more slowly (1-30 min)?

Answer 30

-low pressure receptor-mediated reflex (stretch receptors)-venous side only-atrial natriuretic factor-capillary fluid transfer- vascular stress relaxation- renin-angio system

Question 31

What does vasopressin do?

Answer 31

It’s a vasoconstrictor and can increase arterial pressure via constriction of arterioles and veins.

Question 32

Describe regulation of AP via cardiopulmonary (low pressure) receptors and reflex activity.

Answer 32

increased plasma volume causes increased filling pressure, increased AP via increased CO, and atrial pressure/stretch.Increased atrial pressure/ stretch then causes decreased renal sympathetic activity and decreased vasopressin secretion causing increased renal fluid output

Question 33

Describe regulation of AP via release of atrial natriuretic peptide (ANP).

Answer 33

increased plasma volume causes increased filling pressure, increased AP via increased CO, and increased atrial pressure/stretch. Increased atrial stretch causes release of ANP leading to increased renal fluid output

Question 34

Describe regulation of AP via capillary filtration

Answer 34

increased plasma volume leads to increased arterial (via CO increase) and atrial pressure.Increased arterial pressure causes baroreceptors to be activated, decreasing sympathetic activity and vascular (arteriolar) resistance leading to increased capillary pressure.Increased atrial pressure also leads to increased capillary pressure. Increased capillary pressure leads to increased capillary filtration, lowered blood volume, and finally decreased arterial pressure

Question 35

T or F. When stretched, venous smooth muscle cells have the capacity to relax.

Answer 35

T.

Question 36

Describe regulation of AP via stress relaxation.

Answer 36

increased plasma volume increased arterial pressure and venous pressure. Increased venous pressure leads to:-increased stress relaxation-leading to higher unstressed volume -decreased filling pressure-decreased CO and finally decreased AP

Question 37

Describe regulation of AP via renin-angio system.

Answer 37

decreased arterial pressure leads to increased renin output causing conversion of angiotensinogen to angio I, then ACE makes angio II causing arteriolar/venous constrictionangio II also causes production of aldosterone leading to decreased renal fluid output and then increased blood volume leading to increased arterial pressure

Question 38

What does a renal function curve define?

Answer 38

renal fluid output (y) as a function of arterial pressure (x)

Question 39

Describe the renal function curve.

Answer 39

sigmoidal curve with very steep slope. Means its very sensitive to small changes in MAPThe curve indicates that increasing arterial pressure increases fluid output via a mechanism termed “pressure diuresis”. It is important to note that in a normotensive individual, the curve, as shown here, has a steep slope such that a few mm increase of arterial pressure increases fluid output by several fold.

Question 40

What is a fluid intake line?

Answer 40

Similar to the analysis of cardiac output where steady state output was defined by the intersection of the cardiac and vascular function curves, steady state arterial pressure is defined by the point of intersection of the renal curve with the fluid intake line.

Question 41

Example of fluid intake line and renal function curve.

Answer 41

Arbitrarily raise the arterial pressure from the steady state value (point of intersection shown as A) of 100 mm Hg to 102 mm Hg. We also assume that fluid intake and renal function remain unchanged and therefore the steady state point remains at 100 mm Hg, whereas actual arterial pressure is now 102 mm Hg. At 102 mm Hg arterial pressure, the renal function curve indicates a renal fluid output #2 (point B), much greater than the output at 100 mm, labeled as output #1. Therefore, if fluid output exceeds fluid intake, there will necessarily be a reduction of blood volume, i.e. a case of hypovolemia will occur. This will cause a decrease of cardiac output via the cardiac function/vascular function curves. A decrease of cardiac output will be associated with a reduction of arterial pressure. Thus, over a period of 24 to 48 h, arterial pressure will gradually decrease, until it reaches the steady state pressure of 100 mm Hg. When the pressure reaches 100 mm Hg, it will stop changing further because at this point, and this point only, fluid output exactly matches fluid intake and blood volume will remain stable and so will arterial pressure, as regulated by the kidneys.`

Question 42

Last slide in bulletpoint form.

Answer 42

-increased fluid intake-fluid intake exceeds fluid output leading to increased blood volume-filling pressure increases-causing CO to rise and thus AP- AP rises until renal output matches fluid intake

Question 43

What would a right shift of the renal function curve cause?

Answer 43

On the old curve, steady state pressure is determined to be 100 mm Hg (intersection of renal function curve and intake line). However, on the newly established curve, at 100 mm Hg, there is no significant fluid output. Therefore, fluid intake will exceed fluid output, until the new steady state presure of 106.5 mm Hg is reached, whereupon fluid output again matches fluid intaketakes 24-48 hrs to change

Question 44

Last slide (right shift) in bulletpoint form.

Answer 44

• renal curve right shift- decreased fluid output or increased fluid intake- increased blood volume- increased filling pressure- increased CO- AP rises until fluid output matched fluid intake

Question 45

What things shift the renal function curve to the right?

Answer 45

• angio II- aldosterone- sympathetic activity- vasopressin- renal disease- obesity - kidney removal- old age

Question 46

What things shift the renal function curve to the left?

Answer 46

-ANP, NO, some prostaglandins-diuretics-b-blockers

Question 47

How does increased salt intake lead to increased fluid intake?

Answer 47

via thirst control mechanisms that are centrally mediated

Question 48

How does the renal function curve change in someone who has salt sensitive HTN?

Answer 48

has a slope that is less steep than that of one with a normal curve. If the curve is normal, i.e. has a steep slope, even a several fold increase of salt intake will only result in an increase of arterial pressure of just a few mm Hg, hardly measurable via conventional techniques. Conversely, if the steepness of the slope is lower, then an increase of salt intake will result in increased arterial pressure, although at low salt intake the pressure will be normal

Question 49

How does the renal function curve change with renal disease (and aging)?

Answer 49

the renal function curve not only moves to the right but also becomes less steep. Thus, the individual will not only be hypertensive but also salt sensitive.

Question 50

The concept that a blood volume increase induced by the kidneys is the first event in hypertension has been criticized. Why?

Answer 50

On the basis of findings in humans that blood volume does not seem to be significantly increased in most cases of essential hypertension

Question 51

What is the sequence of events following a right shift of the renal function curve?

Answer 51

1) Significant increase of blood volume within 24 to 48 h. This increase was associated with increased CO and increased AP but decreased TPR, secondary to baroreceptor activation and decreased sympathetic activity. 2) (After about 14 days) Followed by a reduction of CO and an increase of TPR, with two reasons underlying these events. so in HTN, CO is normal but TPR is high in the long run leading to high AP

Question 52

What causes the secondary reduction of CO and increase in TPR seen in right shift of the renal function curve?

Answer 52

Firstly, baroreceptors adapted to the elevated arterial pressure, thus normalizing sympathetic activity. Secondly, a phenomenon termed “whole body autoregulation” occurred.

Question 53

What is whole body auto regulation?

Answer 53

Increased organ perfusion rate causes an autoregulatory increase of organ vascular resistance, thus decreasing total flow (i.e. cardiac output) but increasing TPR. Nevertheless the arterial pressure remained elevated because it was solely determined by the intersection of the renal function curve and the fluid intake line. Thus, elevated pressure does not necessarily predict the actual underlying hemodynamic situation that results in a particular pressure; that is, one can have an infinite number of cardiac output values which when multiplied by the appropriate value for TPR will yield a particular arterial pressure. Essentially, renal pressure diuresis is only regulated by arterial pressure, and not by the underlying hemodynamic variables that create that pressure.

Question 54

What determined filling pressure?

Answer 54

blood volume and compliance

Question 55

Overview of blood regulation.

Answer 55

The cardiac function curve, together with the vascular function curve determines both cardiac output and atrial pressure. Cardiac output, together with TPR determines arterial pressure (AP), which, via the renal function curve (pressure diuresis/ natriuresis mechanism), regulates renal fluid excretion and therefore blood volume and arterial pressure. Additional control mechanisms involve receptors that monitor atrial/venous pressure. Increased atrial pressure causes hormonal and reflex changes via low pressure cardiopulmonary receptors. Thus, we get inhibition of sympathetic activity (dashed line. This causes decreased TPR (reducing arterial pressure) as well as increased renal water excretion, thus reducing blood volume (also decreasing arterial pressure). Renal water excretion is also increased by decreased circulating levels of antidiuretic hormone and increased levels of atrial natriuretic peptide. Arterial pressure regulates sympathetic and parasympathetic activity via baroreceptors and also influences the release of hormones, principally that of angiotensin-aldosterone via baroreceptors (dashed line indicating an increase of arterial pressure decreases the levels of angiotensin-aldosterone). Angiotensin II also increases TPR and decreases renal fluid excretion, as does aldosterone. Finally, the schematic shows the effect of acutely increased arterial pressure on blood vessel tone (increased) via autoregulation which then increases TPR. Chronically increased arterial pressure also causes increased TPR via hypertrophy (thickening of the blood vessel wall, thus causing a decrease of radius and therefore increased resistance) as well as rarefaction (loss of blood vessels, also ultimately causing increased resistance).

Question 56

What are some things that cause normal arterial pressure going from mostly via increases in CO (with compensation with low TPR or vice versa) to mostly increases in TPR?

Answer 56

-Beriberi (CO is very high and TPR is very low)-AV shunts-Hyperthyroidism-Anemia-Pulmonary disease-Paget’s diseaseNormal CO and TPR-Limb removal-Hypothyroidism (TPR is very high and CO is low)

Question 57

What happens with aortic stenosis?

Answer 57

associated with systolic murmur due to increased velocity of blood across the aortic opening leading to high EDV and low SV. The murmur is heard in crescendo decrescendo manner.

Question 58

What is aortic regurgitation?

Answer 58

leaky aortic valve which causes a very rapid decrease in aortic pressure following systole due to backflow. Diastolic murmur can be heard. associated with low SV, high pulse pressure due to lower diastolic pressure, and high ventricular end diastolic volume

Question 59

What is mitral stenosis?

Answer 59

associated with increased left atrial pressure and a diastolic murmur, due to the high velocity of blood flow, resulting in turbulence and a murmur

Question 60

What is mitral regurgitation?

Answer 60

atrial pressure rises during systole, duck to back flow. Systolic murmur heard