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Cardiology > Hypertension Physiology > Flashcards

Hypertension Physiology Flashcards

1
Q

What is hypertension?

A

consistantly high blood pressure of at least 140/90

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2
Q

Primary hypertension is from what?

A

Idiopathic- genetic for example

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3
Q

Causes of secondary hypertension?

7

A
  1. Obstructive sleep apnea
  2. Kidney problems
  3. Adrenal gland tumors -Pheochromocytoma
  4. Thyroid problems
  5. Certain defects in blood vessels you’re born with (congenital) -aortic coarctation
  6. Certain medications, such as birth control pills, cold remedies, decongestants, over-the-counter pain relievers and some prescription drugs
  7. Illegal drugs, such as cocaine and amphetamines
  8. Alcohol abuse or chronic alcohol use
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4
Q

Physiological mechanisms involved in development of essential (primary) hypertension?
4

A
  1. Autonomic nervous system
  2. Cardiac output
  3. Peripheral resistance
  4. Renin-angiotensin-aldosterone system (RAAS)
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5
Q

Other factors/proteins that affect physiology of hypertension?
4

A
  1. ANP (atrial natriuretic peptide)
  2. Bradykinin
  3. Endothelin
  4. EDRF (endothelial derived relaxing factor) or nitric oxide
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6
Q

What is the systolic pressure?

A

The systolic pressure is the force that blood exerts on the artery walls as the heart contracts to pump out the blood.

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7
Q
  1. High ______ pressure is known to be a greater risk factor than _______ pressure for heart, kidney, and circulatory complications and for death, particularly in middle-aged and elderly adults?
  2. What comparison should we watch out for b/w systolic and diastolic BP?
A
  1. systolic
    diastolic
  2. The wider the spread between the systolic and diastolic measurements, the greater the danger.
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8
Q

What is the diastolic pressure?

A

The diastolic pressure is the measurement of force as the heart relaxes to allow the blood to flow into the heart.

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9
Q

HIgh diastolic pressure is a strong predictor of _____ _____ and ______ in young adults?

A

heart attack and stroke

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10
Q

Why do we want diabetics on an ACE?

A

renal protective

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11
Q

What is the mean arterial blood pressure?

What does it describe?

A

MAP = (CO*SVR) - CVP
(Cardiac output X systemic vascular resistance) - central venoud pressure

As blood is pumped out of the left ventricle into the arteries, pressure is generated. MAP is this pressure.

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12
Q

What is the arterial pulse pressure?

What is it an indicator for? 2

A

Pulse pressure is the difference between the systolic and the diastolic readings during ejection.

It appears to be an indicator of

  1. stiffness and
  2. inflammation in the blood-vessel walls.
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13
Q
  1. What makes stiffer and more injured the vessels?
  2. Although not yet used by providers to determine treatment, evidence suggests that it may prove to be a strong predictor of _____ ______, particularly in _____ adults.
  3. Some studies suggest that in people over 45 years old, every ___ mm Hg increase in pulse pressure increases the risk for _____ rises by 11%, ___________ _______ by 10%, and overall _______ by 16%. (In younger adults the risks are even higher.)
A
  1. The greater the difference between systolic and diastolic numbers
  2. heart problems
    older
3. 
10
stroke
cardiovascular disease
mortality
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14
Q

What is Peripheral Vascular resistance (PVR)?

The resistance offered by the peripheral circulation is known as ?

A

A term used to define the resistance to flow that must be overcome to push blood through the circulatory system.

the systemic vascular resistance (SVR).

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15
Q

Neural Mechanisms that affect blood pressure

4

A
  1. ANS
  2. Intrinsic mechanisms
  3. Extrinsic mechanisms
  4. CNS
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16
Q

How does the ANS affect blood pressure? 3

What instrinsic mechansims affect BP? 2

What extrinsic mechanisms affect BP? 3

How does the CNS affect BP? 1

A

ANS:

  1. Intrinsic circulatory reflexes,
  2. Extrinsic reflexes, and
  3. higher neural control

Intrinsic:

  1. Baroreceptors and
  2. Chemoreceptors

Extrinsic:

  1. Pain,
  2. Cold,
  3. Isometric exercises

CNS:
1. Change in mood or emotion

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17
Q
  1. Sympathetic and Parasympathetic Divisions of ____.
  2. Contributes through the control of CV function through modulation of ______ and _______ function.
  3. Where are these located?
  4. What are the centers called that control these? 2
A
  1. ANS
  2. cardiac
    vascular
  3. Medulla oblingata
  4. Vasomotor Center
    Cardioinhibitory Center
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18
Q

ARTERIAL BARORECEPTORS
1. The most important arterial baroreceptos are located where? 2

  1. What do they respond to?
  2. As arterial pressure suddenly rises, the walls of these vessels passively _____, which stimulated the _____ of these receptors.
  3. What does this inhibit?
A
  1. the carotid sinus and in the aortic arch.
  2. They respond to stretching of the arterial wall.
  3. expand
    firing
  4. Inhibits central sympathetic discharge.
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19
Q

Where is the carotid sinus located?

A

(at the bifurcation of the external and internal carotids)

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20
Q

ARTERIAL BARORECEPTORS
1. The _____ ______is the most important for regulating arterial pressure.

  1. _____ _____ receptors have a higher threshold pressure and are less sensitive than the _____ _____ receptors?
A
  1. carotid sinus
  2. Aortic arch
    carotid sinus
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21
Q

If you reduce ______ pressure you will also reduce the _____ pressure?

A

systolic

diastolic

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22
Q

What is responsible for rapid moment to moment adjustments in B/P and change in position?

With chronic changes, the baroreceptors tend to “reset” to adjust to the increasing ___ or ______ ______ and are not as good at regulating the mechanisms to cause a _______in sympathetic activity.

A

Postural Baroreflex
(arterial baroreceptors)

CO
arterial pressure
decrease

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23
Q

What innervated the aortic arch receptors?

What innervated the carotid sinus receptors?

A

Vagus nerve X

Carotid sinus nerve to Nerve IX

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24
Q

Chemoreceptors are sensitive to changes in what?
3

The ones that control BP are loacted where?

They communicate with the vasomotor center and can induce what?

A
  1. oxygen,
  2. carbon dioxide, and
  3. hydrogen ion concentration in the blood

Located in the
—carotid bodies
which lie in the bifurcation of the two common carotids and the aortic bodies of the aorta

vasoconstriction

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25
Q

Autonomic Regulation of Cardiac Function is controlled sympathetically (2) and parasympathetically (1) by what?

A

Sympathetic: SA and AV Nodes

Parasympathetic: Vagus Nerve

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26
Q

Sympathetic nervous system stimulation can cause both _______ _______ and _______ ________.

The ____ has an important role in maintaining a normal blood pressure.

A

arteriolar constriction
arteriolar dilation

ANS

27
Q

Parasympathetic Nervous system contributes to the regulation of ______ _______, but has little control over the _____ _______.

A

heart function

blood vessels

28
Q

Autonomic Neurotransmitters:

_________ is the postganglionic neurotransmitter for parasympathetic neurons.
__________ is the main neurotransmitter for postganglionic sympathetic neurons.

A

Acetylcholine

Norepinephrine

29
Q

What kind of receptors does Acetylcholine bind with?

What kind of receptors does Norepinephrine bind with?

A

Acetylcholine (parasympathetic): Cholinergic receptors

Norepinephrine (sympathetic): Adrenergic receptors

30
Q

What are the two types of adrenergic receptors?

In vascular smooth muscle, stimulation of ______ receptors produces vasoconstriction and stimulation of _____ receptors causes vasodilation

A

alpha and beta

alpha
beta

31
Q

Although there is little evidence to suggest that epinephrine and norepinephrine have any clear role in hypertension, their effects are important, at least because why?

Because catecholamines act on the heart and blood vessels through alpha and beta adrenoceptors, the CV actions of catecholamines can be blocked by treatment with ____ _______ and ____ ______?

It is probable that HTN is related to an interaction between the ____ and the _____ system along with other factors.

A

drugs that block the sympathetic nervous system do lower B/P and have a well established therapeutic role.

alpha-blockers and beta blockers.

ANS
RAAS

32
Q

What are the parts of the CNS that affect blood pressure?
2

Autonomic Response to Circulatory Stresses are what? 3

A

CNS Ischemic Response
Cushings Reflex

Postural Stress
Valsalva’s Maneuver
Face Immersion

33
Q

What is the equation for BP?

A

Cardiac Output x Peripheral Vascular resistance

34
Q

Most people with essential HTN have a normal ______ ______ but a raised _____?

It has been postulated that in very early hypertension the PVR is not raised and the elevation of the blood pressure is caused by a raised cardiac output, which is related to sympathetic overactivity.

The subsequent rise in peripheral arteriolar resistance might therefore develop in a compensatory manner to prevent the raised pressure being transmitted to the capillary bed where it could substantially affect cell homeostasis.

A

cardiac output
PVR (peripheral vascular resistance)

egg before the chicken or chicken before the egg?

35
Q
  1. PVR is determined not by large arteries or the capillaries, but by ______ ________, the walls of which contain ______ ______ cells.
  2. Contraction of smooth muscle cells is thought to be related to a rise in_______ ________ _________.
  3. Prolonged smooth muscle constriction is thought to induce structural changes with ________ of the arteriolar vessel walls possibly mediated by _______, leading to an irreversible rise in PVR.
  4. This may explain the vasodilatory effect of drugs that block the _______ ______.
A
  1. small arterioles
    smooth muscle
  2. intracellular calcium concentration
  3. thickening
    angiotensin
  4. calcium channels. (Calcium channel blockers)
36
Q

The Renin-angiotension-aldosterone system:

  1. Where exactly is renin released from?
  2. What causes its release? 3
  3. What are functions of renin release? 2
A
  1. kidneys
    • -decreased blood flow,
    • -decreased pressure, and
    • -increased sodium
  3. regulates blood volume and systemic vascular resistance
37
Q

The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating _____ ______ and _______ _______ ______, which together influence cardiac output and arterial pressure.

There are three important components to this system. What are they?

What stimulates the formation of angiotensin and what is it primarily released by?

What does angiotensin stimulate the release of and from where?

A

blood volume
systemic vascular resistance

1) renin
2) angiotensin
3) aldosterone

Renin (and angiotensinogen-renin cleaves it), which is primarily released by the kidneys,

stimulates the formation of angiotensin in blood and tissues,

which in turn stimulates the release of aldosterone from the adrenal cortex.

38
Q

What does renin convert?

What does ACE convert?

A

angiotensinogen to angiotensin 1

angiotensin 1 to angiotensin 2

39
Q

Where is renin secreted in the kidney?

It is released in response to what? 3

A

Renin is secreted from the juxtaglomerular apparatus of the kidney located in the wall of the afferent arteriole.

Renin is released in response to

  1. glomerular underperfusion or
  2. a reduced salt intake.
  3. It is also released in response to stimulation from the sympathetic nervous system.
40
Q
  1. ___________ _____associated with the afferent arteriole entering the renal glomerulus are the primary site of renin storage and release in the body.
  2. A reduction in_______ ______ _______ causes the release of renin from the JG cells, whereas increased ______ inhibits renin release.
  3. _____________ located on the JG cells respond to sympathetic nerve stimulation by releasing renin.
  4. Specialized cells (macula densa) of distal tubules lie adjacent to the JG cells of the afferent arteriole. What are the function of these cells? 2
A
  1. Juxtaglomerular (JG) cells
  2. afferent arteriole pressure
    pressure
  3. Beta1-adrenoceptors
  4. The macula densa
    senses the amount of
  5. sodium and
  6. chloride ions in the tubular fluid.
41
Q
  1. When NaCl is elevated in the tubular fluid, renin release is _______. In contrast, a reduction in tubular NaCl ______ renin release by the JG cells.
  2. There is evidence that _________ stimulate renin release in response to reduced _____ transport across the macula densa.
  3. When afferent arteriole pressure is _______, glomerular filtration decreases, and this ______ NaCl in the distal tubule.
  4. This serves as an important mechanism contributing to the release of renin when there is afferent arteriole _________.
A
  1. inhibited
    stimulates
  2. prostaglandins
    NaCl
  3. reduced
    reduces
  4. hypotension
42
Q
  1. When renin is released into the blood, it acts upon a circulating substrate, __________, that undergoes proteolytic cleavage to form the ________, _________ _.
  2. Vascular endothelium, particularly in the lungs, has an enzyme,________ ________ ______, that cleaves off two amino acids to form the _______, _______ ___, although many other tissues in the body (heart, brain, vascular) also can form ___.
  3. Angiotenin II is a potent__________ and thus causes a rise in B/P.
A
  1. angiotensinogen
    decapeptide, angiotensin I
    • angiotensin converting enzyme (ACE)
    • octapeptide, angiotensin II (AII)
    • AII
  3. vasoconstrictor
43
Q

Angiotension II has several very important functions. WHat are they?
5

A
  1. Constricts resistance vessels (via AII receptors) thereby increasing systemic vascular resistance and arterial pressure.
  2. Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention
  3. Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary, which increases fluid retention by the kidneys.
  4. Stimulates thirst centers within the brain.
  5. Facilitates norepinephrine release from nerve endings and inhibits norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic function.
  6. constricts vessels and increasing resistance and pressure
  7. releases aldosterone and increases Na+ and fluid retention
  8. Releases ADH/vassopression which increases fluid retention
  9. stimulates thirst centers
  10. releases norepi into the blood stream
44
Q

What is the major target of aldosterone?

What does it stimulate there?

A

The major target of aldosterone is the distal tubule of the kidney,

where it stimulates exchange of sodium and potassium.

45
Q

Three primary physiologic effects of aldosterone result are?

A
  1. Increased resorption of sodium: sodium loss in urine is decreased under aldosterone stimulation.
  2. Increased resorption of water, with consequent expansion of extracellular fluid volume. This is an osmotic effect directly related to increased resorption of sodium.
  3. Increased renal excretion of potassium.
46
Q

The two most significant regulators of aldosterone secretion are what?

A

Angiotensin II

Concentration of potassium ions in extracellular fluid

47
Q

How do the following regulate aldosterone:

Angiotensin II?

Concentration of potassium ions in extracellular fluid?

A

Activation of the renin-angiotensin system as a result of decreased renal blood flow results in release of angiotensin II, which stimulates aldosterone secretion.

Small increases in blood levels of potassium strongly stimulate aldosterone secretion.

48
Q

ACE inhibitors, AII receptor blockers and aldosterone receptor blockers, for example, are used to decrease what three things?

A
  1. arterial pressure,
  2. ventricular afterload,
  3. blood volume
49
Q

The decrease in arterial pressure, ventricular afterload, and blood volume decrease _______ ______ as well as inhibit and reverse ______ and ________ _________.

A

ventricular preload

cardiac and vascular hypertrophy.

50
Q

The circulating renin-angiotension system is not always directly responsible for the rise in B/P in essential hypertension.

Many hypertensive patients have low levels of renin and angiotensin II (especially _____ and ______ _______) and drugs that block the renin-angiotension system are not particularly effective for them.

Often with these populations, this is better managed with ______, ______ ______ ______ or ____ _______.

A

elderly and African Americans

diuretics, calcium channel blockers or beta blockers.

51
Q

Long Term Control Mechanisms of BP?

4

A

Renal-Body Fluid System
Renal Output Curve
Pressure diuresis
Pressure natriuresis

52
Q

The renin-angiotensin-aldosterone pathway is regulated not only by the mechanisms that stimulate renin release, but it is also modulated by ______ ________ (____ and ____)released by the heart.

These ________ ________ acts as an important counter-regulatory system for the RAAS.

A

natriuretic peptides (ANP and BNP)

natriuretic peptides

53
Q

Natriuretic peptides are involved in the long-term regulation of what? 2

Two major pathways of natriuretic peptide actions are?

A
  1. sodium and water balance,
  2. blood volume and arterial pressure.

1) Vasodilator effects
2) Renal effects that lead to natriuresis and diuresis

54
Q

What kind of vasodilator effects do natriuretic peptides have? 3

Natriuretic peptides have renal effects that lead to natriuresis and diuresis. What does this do? 4

A
  1. Dilate arteries and veins
  2. Decrease systemic vascular resistance
  3. Reduce cardiac output
  4. Increase glomerular filtration rate
  5. Increase sodium and fluid excretion
  6. Spare potassium
  7. Decrease renin release
55
Q

What is ANP?

It is released in response to what? 3

A

Atrial natriuretic peptide (ANP)
is a hormone from the atria of the heart in response to atrial distension due to
1. increased blood volume,
2. angiotensin II stimulation,
3. endothelin and sympathetic stimulation (beta-adrenoceptor mediated).

56
Q

What is the function of ANP?

A defect in this system may cause (2)?

A

Its effect is to increase sodium and water excretion from the kidney as a sort of natural diuretic.

A defect in this system may cause

  1. fluid retention and
  2. hypertension.
57
Q

What is BNP?

Where is it synthesized? 2

A

Brain-type natriuretic peptide (BNP)
Released by the same mechanisms that release ANP
Acts similarly to ANP

Synthesized within the ventricles, as well as the brain

58
Q

Endothelial dysfunction:
Vascular endothelial cells play a key role in CV regulation by producing a number of potent local vasoactive agents. What are these?

A

1) Nitric oxide (vasodilator)

2) Endothelin (vasoconstrictor)

59
Q
  1. What is nitric oxide produced by?
  2. It diffuses through what and into what to cause vasodilation?
  3. What does endothelin produce?
    What does it activate?
  4. It also affects?
A
  1. Nitric oxide is produced by arterial and venous endothelium 2. through the vessel wall into the smooth muscle causing vasodilatation.
  2. Endothelin produces a salt sensitive rise in blood pressure
    and also activates local renin-angiotensin systems.
  3. Also effects intracellular calcium (too much)
60
Q

Bradykinin is what kind of substance?

What is it inactivated by?

How do ACE inhibitors affect bradykinin?

This increase in Bradykinin causes the _______ associated with ACE inhibitor therapy

A

Vasoactive substances (potent vasodilator)

It is inactivated by angiotensin converting enzyme.

ACE inhibitors may exert some of their effect by blocking the bradykinin inactivation.

cough

61
Q

How does HTN cause hypercoagulability?

5

A
  1. abnormalities of vessel wall (endothelial dysfunction and damage),
  2. abnormal blood constituents,
  3. abnormal levels of homeostatic factors,
  4. abnormal platelet activation and fibrinolysis, and
  5. abnormal blood flow

suggesting that HTN confers a prothrombotic or hypercoaogulable state. These components appear to be related to target organ damages.

62
Q

Vasodilating systems?

5

A
  1. Parasympathetic
  2. Kallikrein-kinin system
  3. Prostaglandins
  4. Endothelial derived relaxant factor
  5. Atrial natriuretic factor
63
Q

Vasoconstricting systems?

7

A
  1. Sympathetic
  2. Calcium
  3. local renin-angiotensin system
  4. circulating renin-angiotensin system
  5. endothelin
  6. Ouabain
  7. Vasopressin (probs)
64
Q

Vascular growth factors?

4

A
  1. insulin growth factor
  2. growth hormone
  3. PTH
  4. Tissue oncogenes

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