Unit 7 - Long term control of blood pressure Flashcards Preview

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Flashcards in Unit 7 - Long term control of blood pressure Deck (29)
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1
Q

what are the set points for hypotension and hypertension? what if it’s transient VS chronic?

A

hypo: low BP where systolic is less than 90 mmHg
HTN: sustained above 140/90
-transient are normal, from fever, exercise, emotions
-chronic is major cause of heart failure, vascular disease, renal failure, and stroke

2
Q

what is the most important regulator of MAP set point?

A

RAAS

-major regulation of total Na+ content and long-term MAP, ANS, ADH, and ANP

3
Q

what are fast VS intermediate VS slow factors that change arterial blood pressure/

A

fast: baroreceptor reflex (cardiac and vascular)
- adapts to long-term changes and effects are blunted (low gain)
intermediate: renal actions (PVR)
slow: renal salt and water excretion

there are many things in the acute response, but less so in the chronic response

4
Q

how does the kidney directly and indirectly act on blood pressure?

A

maintains long term BP

  • direct: alters blood volume
  • indirect: RAAS mechanism with juxtaglomerular apparatus
5
Q

what do macula densa, juxtaglomerular cells, and mesangial cells do? (entire juxtaglomerular apparatus)

A

MD: collective name for specialized group of epithelial cells in initial part of distal tubules; sense osmolarity changes
JX: granular cells that make renin
MC: provide anchor, may be involved in response to hypotension since they have actin and myosin, and act under sympathetic stimulation

6
Q

what are local VS global effects of RAAS?

A

local are more important, but global are more known

  • many tissues have local RAAS that is less understood, but provides local control of hemodynamics
  • global has almost unlimited capacity, and is not a neural reflex
7
Q

what are 3 determinants of renin secretion?

A
  1. neural baroreceptors signal via renal sympathetics to granular cells in JGA
  2. intrarenal baroreceptors in afferent arterioles (granular cells)
    - can function w/o innervation
  3. NaCl delivery to MD of JGA
    - osmotic swelling releases transmitter that inhibits renin secretion

this system is very redundant, meaning it’s very important

8
Q

autoregulation of JGA if decreased arterial pressure?

A

decreased MAP causes decreased glomerular hydrostatic pressure, which decreases GFR, and decreases flow rate in the LoH which increases NaCl resorption

  • decreased MD NaCl causes increases renin and decreased arteriole resistance/tone
  • -increased renin causes more AII and efferent arteriole resistance/tone, causing increased GFR
  • -decreased AA resistance/tone causes increased GFR
9
Q

mechanism of RAAS?

A
  1. renin from juxtaglomerular cells is proteolytic enzyme that acts on angiotensin (liver plasma alpha2-globulin) to convert to angiotensin I (decapeptide)
  2. ACE from lungs converts to angiotensin II (octapeptide)
10
Q

what are three critical functions of AII?

A
  1. powerful vasoconstricter to increase peripheral vascular resistance
  2. constricts mesangial cells to reduce GFR
  3. stimulates aldosterone secretion (stimulate proximal Na/H exchange, increase blood volume via pressure naturesis and diuresis)
11
Q

does AII have negative or positive feedback on granular/juxtaglomerular cells?

A

negative feedback to inhibit renin production by granular cells
-bind to AT receptor to decrease intracellular Ca to inhibit renin

12
Q

what is ultimately responsible for maintaining BP setpoint in longterm? shortterm?

A

kidneys longterm, baroreceptor reflex short term
-sympathectomy has little impact, exccept in resistant HTN
-

13
Q

what is renal nerve ablation’s effect?

A

“purported” cure for resistant HTN (ablate from ilaic –> femoral –> renal arteries will drop BP)
-but no significant change from ablation and sham procedures

14
Q

what are the main factors influencing blood pressure? the equation?

A

BP varies directly with cardiac output, peripheral resistance, blood volume
-BP = CO x PVR

15
Q

what is ECF determined by? what is the osmotic content of Na?

A

total osmotic content; 90% Na

16
Q

how do the kidneys know about Na+ content?

A

indirectly sensed

17
Q

what are some effectors of Na content?

A
  1. change in GFR - sympathetic nerve activity (minor), and AII (major)
  2. ADH and ANP sometimes
18
Q

what are factors that control aldosterone?

A

circulating level of AII

  • minor factors are plasma K concentration and ANP
  • stimulates Na+ reabsorption in cortical connecting tubules and collecting ducts
  • -influences about 2% of total filtered Na+
19
Q

why are chronic diseases of PCT not usually seen?

A

b/c such a huge part of monitoring Na level, that if there is a disease they will die very quickly due to hypovolemia

20
Q

what is tubuloglomerular feedback?

A

acts in opposite direction to other reflexes in order to blunt effectiveness and prevent “over-correction”
-effects do NOT predominant, but blunts the increase in renal blood flow and GC

21
Q

what are naturetic peptides?

A

ANP and BNP

  • inhibit release of renin
  • relax afferent arteriole
  • used diagnostically
22
Q

out of these, which increase and decrease Na+ reaborption?

  • cortisol
  • progesterone
  • estrogen
  • GH
  • TH
  • insulin
  • glucagon
  • PTH
A

increase Na reabsorption: cortisol, estrogen, GH, TH, insulin
decrease Na reabsorption: progesterone, PTH

23
Q

how do baroreceptors and osmoreceptors control water excretion?

A

B: assess vascular fullness
O: assess plasma osmolarity

24
Q

how do proximal and distal nephron compare in water control?

A

proximal: regulates ECF based on BP
- affects Na and water together
distal: determined by ADH (major regulator of total body water)
- aldosterone and ADH affect Na and water excretion independently

25
Q

what is the Guyton hypothesis?

A

abnormal renal Na handling in the pathogenesis of HTN

26
Q

what are causes of secondary HTN?

A
  • renal disorders
  • endocrine disorders
  • endogenous medications and drugs
  • pregnancy
  • coarctation of the aorta
  • neurologic disorders
  • psychosocial factors
  • intravascular volume overload
  • systolic HTN
27
Q

how can obesity and insulin resistance cause increased blood pressure?

A

unknown mechanism, but causes hyperinsulinemia that can affect kidney, smooth muscle proliferation, and SNS

  • kidney will increase Na+ reabsorption
  • smooth muscle cell proliferation causes vasoconstriction
  • increased SNS activity causes increased CO and vasoconstriction
28
Q

what are the drugs that block renin?

A
  1. beta-blockers
  2. alpha-agonists
  3. aliskirin
29
Q

what are drugs that block aldosterone?

A

spironolactone

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