Urinary: Control of Blood Pressure (ECF volume) Flashcards Preview

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Flashcards in Urinary: Control of Blood Pressure (ECF volume) Deck (11)
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1
Q

What is the baroreceptor reflex?

A

Baroreceptors on aortic arch and carotid sinus sense stretch and signal to change HR or TPR.

Rapidly changes BP, but only good for acute changes as sustained increases reset the threshold.

2
Q

What are the 4 neurohumoral pathways controlling ECF volume and therefore blood pressure?

A
  • Renin angiotensin aldosterone system
  • Sympathetic NS
  • Anti diuretic hormone
  • Atrial natriuretic peptide
3
Q

Outline how the renin angiotensin aldosterone system works to change blood pressure

A

Produces angiotensin 2 which causes:

  1. Vasoconstriction to increase TPR
  2. Stimulates Na+ reab in kidney
    Vasoconstricts AA and EA causing enhanced Na+ reab in the PCT via the N-H exchanger
  3. Stimulates release of aldosterone from adrenal cortex
    Aldosterone acts on principal cells of CD to simulate Na+ reab
    Also activates ENaC and apical K+ channels
4
Q

What is renin and what factors stimulate its release?

A

Renin is a proteolytic enzyme that is released from GRANULAR cells of the juxtaglomerular apparatus. It cleaves angiotensin into angiotensin 1.

Released when:

  • reduced NaCl delivery to distal tubule
  • reduced perfusion pressure in kidney
  • sympathetic stimulation of juxtaglomerular apparatus
5
Q

What is the affect of ACE on bradykinin?

A

Bradykinin has vasodilator actions. ACE breaks is down into peptide fragments therefore further enhancing the vasoconstriction.

6
Q

How does the sympathetic NS act to alter blood pressure?

A
  • Sympathetic stimulation reduces renal blood flow by vasoconstricting AA and EA.
  • Activates apical Na-H and basolateral Na-K-ATPase in PCT to enhance Na+ reabsorption.
  • Stimulates renin release
7
Q

How does ADH affect BP?

A

ADH is released when plasma osmolarity increases or there is severe hypovolaemia.

It stimulates Na+ reabsorption on the thick ascending limb by stimulating the Na-K-2CL cotransporter.

Increases water reabsorption

8
Q

What is atrial natriuretic peptide?

A

A peptide synthesised and stored in atrial myocytes. Its release in response to stretch - causes a fall in BP

9
Q

How does atrial natriuretic peptide affect BP?

A

Decreases BP by:

  • vasodilating AA to increase GFR
  • inhibits Na+ reab along the nephron
  • causes natriuresis (loss of sodium in urine)

If circulating volume is low ANP release is inhibited to support BP.

10
Q

What is the affect of NSAIDs on prostaglandins?

A

NSAIDs inhibit the cyclo-oxygenase pathway involved in the formation of prostaglandins
Prostaglandins usually reduce Na+ reab and buffer excessive vasocontriction produce by SNS and RAAS.

Therefore giving NSAIDs when renal perfusion is already compromised can lead to acute renal failure

11
Q

How does dopamine affect BP?

A

Decreases BP:
There are dopamine receptors on renal BV and cells of PCT and thick asc limb.
It causes vasodilation and increases renal blood flow, and reduce reab of NaCl by inhibting NH exchanger and Na-K-ATPase

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