Blood Pressure Flashcards

1
Q

How is blood pressure regulated in the short term?

A

Baroreceptor reflex
(Adjust sympathetic and parasympathetic input to the heart to alter CO, adjust sympathetic input to peripheral resistance vessels to alter TPR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is the blood pressure maintained over medium and longer time periods?

A

Complex interactions of neurohumeral responses

Directed at controlling sodium balance and thus extracellular fluid volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can controlling Na+ levels control plasma volume and ultimately blood pressure?

A

By changing the sodium levels you can change the extracellular fluid volume.
Plasma is part of the extracellular fluid compartment so technically controlling na+ you can control the plasma volume and plasma volume affects heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the four pathways in which there is neurohumoral control over the circulation volume and hence BP?

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiurectic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What factors stimulate the release of renin from the kidneys?

A

A) reduced NaCl delivery to distal tube (the macula densa cells to be precise)

B) reduced perfusion pressure (fall in BP) in the kidney causes the release of renin (detected by baroreceptors in afferent arteriole)

C) sympathetic stimulation to juxtaglomerular apparatus increases release of renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is renin released from?

A

Granular cells of juxtaglomerular apparatus in the kidneys (JGA)

These granular cells surround the afferent arteriole entering the glomerulus. They are located close to the distal tube which is surrounded by macula dense cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the two types of angiotensin II receptors?

A

AT1 - main actions via this one (gpcr)

AT2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect does angiotensin II have at the following sites:

  1. Arterioles
  2. Kidney
  3. Sympathetic NS
  4. Adrenal cortex
  5. Hypothalamus
A
  1. Vasoconstriction
  2. Stimulates Na+ reabsorption at the kidneys
  3. Increased release of Noradrenaline
  4. Stimulates release of aldosterone
  5. Increases thirst sensation (+ stimulates ADH release)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is aldosterone released from?

A

The adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the actions of aldosterone?

A
  • stimulates Na+ and there water reabsorption
  • activates apical Na+ channels (ENaC= epithelial Na channel) and apical K+ channel
  • increases basolateral Na+ extrusion via Na/K/ATPase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What effect does aldosterone have on potassium?

A

It lower levels of K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is ACE found?

A

Lungs predominantly (in epithelial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does ACE do? (2)

A
  1. It converts angiotensin I to angiotensin II

2. Converts bradykinin to peptide fragments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does ACE’s action on bradykinin help to raise blood pressure?

A

Because bradykinin has vasodilator actions and breaking it down means there is less vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a side effect of ACE inhibitors and why does this happen?

A

Bad/dry cough

If ACE is inhibited then it doesn’t break down bradykinin

The accumulation of bradykinin causes the cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give an example of an ACE inhibitor

A

Captopril, lisinopril, perindopril, enalapril

17
Q

In what way does the sympathetic NS raise blood pressure? (2)

A

Causes vasoconstriction of arterioles=increases BP (short term)

This vasoconstriction decrease the renal blood flow which stimulates Na+ retention which has a long term effect of raising your blood pressure

18
Q

How is Na+ retained by stimulation of the sympathetic NS?

A

Activation of the apical Na/H-exchanger and basolateral Na/K/ATPase in PCT

The lack of blood flow also stimulates the renin release from juxtaglomerular cells leading to increased Ang II levels and aldosterone levels which further increased Na+ reabsorption

19
Q

What is the main function of the ADH?

A

Formation of concentrated urine by retaining water to control plasma osmolarity

It increases water reabsorption in the distal nephrons

20
Q

What is ADH stimulated by?

A

Plasma osmolarity or severe hypovolaemia

21
Q

What system is in place to lower BP over the long term?

A

ANP (atrial Natriuretic peptides)

22
Q

How do ANPs work?

A

Cause vasodilation of afferent arteriole

Increase blood flow to glomerulus

Inhibits Na+ reabsorption

Water retained

BP raised

23
Q

What are prostaglandins?

A

Act as vasodilator locally

(PGE2) Enhance glomerular fitatrion and reduce Na+ reabsorption

Can have important protective function: Act as buffer to excessive vasoconstriction produced by SNS and RAA system

Important when levels of Ang II are high

24
Q

What role does dopamine play in manning blood pressure?

A

Formed locally in the kidneys from circulating L-DOPA

Causes vasodilation and increases renal blood flow

Reduce reabsorption of NaCl (inhibits NaH exchanger and Na/K ATPase in principle cells of PCT and TAL)

25
Q

What clinical use does dopamine have?

A

Used to treat Parkinson’s disease

Will lower BP so need to be aware of that!

Dopamine is not used as an antihypertensive