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5. ADV PHYS > Long term BP > Flashcards

Long term BP Flashcards

1
Q

who controls long term BP:

A

kidney

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2
Q

how long to control long term BP:

A

days - months - yrs

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3
Q

long term BP: intrinsic mechanisms

A

kidney

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4
Q

long term BP: extrinsic mechanisms

A
  • symp nn

- hormonal sys (RAAS, atrial natriuetic hormone, ADH)

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5
Q

long term BP: function

A
  • maintain BP despite changes in CO, TPR, salt intake
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6
Q

body Na+ balance: how is it controlled

A
  • total Na input = rate Na excreted (output)
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7
Q

Na excretion rate=

A

Na filtration rate - Na reabsorption rate

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8
Q

Na approx % reabsorbed:

A

~99% reabsorbed

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9
Q

body Na+ balance: absorption where (2)

A
  • distal tubule

- collecting duct

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10
Q

Na filtration rate altered by:

A
  • GFR (increase = increase Na filtered)
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11
Q

if Na content altered, what is effected?

A

osmolarity Na, Cl- and HCO3 account for 95% of osmolarity in ECF

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12
Q

which (2) sys corrects osmolarity

A
  • osmoreceptors

- ADH (antidiuretic hormone sys)

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13
Q

correcting osmolarity: process

A

ADH changes ECF vol - affect VR - changes CO = BP

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14
Q

kidney role: general

A

balance output of Na to input so Na content (and ECF vol, BP too) remain constant

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15
Q

eg. decrease Na content

A

decreased: ECF - plasma vol = decrease VR - decrease CO = decrease BP

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16
Q

define: diuresis

A

rate excretion of H2O

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17
Q

define: pressure natriuresis

A

rate excretion of Na

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18
Q

eg. if perfusion pressure increased in renal aa.

A
  • both diuresis and pressure natriuresis increase
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19
Q

perfusion pressure is in/extrinsic to kidney?

A

intrinsic (no influence from nn, hormones etc.)

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20
Q

eg. if BP decreased due to TPR/CO, effect and how to return normal?

A
  • decrease in Na + H2O excretion (via pressure diuresis natriuresis process)

= increase total body Na therfore ECF vol, CO and return BP to normal

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21
Q

Guyton’s analysis of pressure natriuresis/ diuresis: straight line rep

A
  • intake of Na
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22
Q

Guyton’s analysis of pressure natriuresis/ diuresis: renal output curve rep

A
  • pressure natriuresis and diuresis
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23
Q

Guyton’s analysis of pressure natriuresis/ diuresis: intersection rep

A
  • equlibrium point

- rate of excretion

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24
Q

Guyton’s analysis of pressure natriuresis/ diuresis: normal conditions- BP at equilibrium

A

100 MAP

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25
Guyton's analysis of pressure natriuresis/ diuresis: if TPR/CO increases BP, features
- output exceeds intake - ECF vol will decrease until reach equilibrium - Na input/output balanced
26
Guyton's analysis of pressure natriuresis/ diuresis: hypertension, curve shifts to
right
27
Guyton's analysis of pressure natriuresis/ diuresis: hypertension, to excrete sufficient Na
- increased BP to balance increase Na intake to help excrete
28
perfusion P in cortical blood v of kidney remains relatively constant despite
- changes in renal aa
29
autoregulation: of and features
- afferent/ efferent arterioles - near constant glomerular filtration rate - protect fragile glomerular capillaries from excessive P
30
pressure natriuresis and diuresis lies where in kidney/ why?
- medulla | - as cortex of kidney not exposed to changes in perfusion P
31
mechanism: increased medullary perfusion response
- involve hydrostatic effects | - actions of paracrine (eg. NO, ATP) released
32
BP in renal aa increases ? in medullary capillaries
perfusion pressure
33
increase shear stress cause release of: in endothelial cells
- release of NO
34
NO features:
- relaxes pericytes that wrap around capillaries = increasing flow - NO circumvents 'autoregulation' of blood flow in medulla
35
increased hydrostatic P in medullary cap forces:
protein free plasma from cap to inter fluid
36
why and how does increased interstitial P in medulla affect renal cortex:
- kidney enclosed in cap resisting stretch | - will increase 'renal inter fluid P' to oppose reabsorption of Na and water by proximal tubules (in cortex)
37
which Na reabsorption transporters inhibited during high medullary perfusion: list (4) and location
- Na/K exchange pump - NHE3: Na/H exchanger (proximal tubule) - NKCC: Na, K, 2Cl co transport (thick ascending LOH, early distal tubule) - ENaC: Na channel (late distal tubule, collecting duct)
38
what (2) Na transporter inhibited by NO:
- Na/K pump | - NKCC (Na, K, 2Cl cotransport)
39
which Na transporter inhibited by ATP released from ?
- released from proximal tubule | - inhibits NHE3 (Na/H exchanger)
40
control Na excretion via hormones: list most important ones (2)
- RAAS: renin angiotensin aldosterone sys | - ANP: atrial natruretic peptide
41
control Na excretion via hormones: RAAS- juxtaglomerular app formed by (location)
- initial portion of distal tubule | - next to aff/eff arterioles
42
control Na excretion via hormones: RAAS- macula densa features
- in jux app region | - specialised epithelial cells of distal tubule
43
control Na excretion via hormones: RAAS- juxtaglomerular cells features
- adjacent to macular densa - derived smooth mm cells in wall of aff arteriole - renin granules act like renal baroreceptors
44
control Na excretion via hormones: RAAS- renin features
- enzyme cleaves off 10 aa from angiotensinogen (from liver) = angiotensin I
45
control Na excretion via hormones: RAAS- angiotensin I reduced into/ by
- reduced to 8 aa form, angiotensin II by ACE (angiotensin converting enzyme) in blood v endothelium (esp lung)
46
control Na excretion via hormones: RAAS- renin activity in plasma determines
- conc of angiotensin II and therfore aldosterone in plasma
47
control Na excretion via hormones: RAAS- renin release by juxtaglomerular cells stimulated by (3)
- low BP detected by central baroreceptors - decreased wall tension in aff arterioles - reduced NaCl conc in distal tubule
48
control Na excretion via hormones: RAAS- renin release detected by/effect: low BP
- detected by central baroreceptors - increased sym output - Ad release
49
control Na excretion via hormones: RAAS- renin release detected by/effect: decreased wall tension
- detected by renal baroreceptors
50
control Na excretion via hormones: RAAS- renin release detected by/effect: reduced NaCl conc
- detected by macula densa cells
51
control Na excretion via hormones: RAAS- NaCl conc sensed by macular densa as
- transport rate of Cl via NKCC in early distal tubule
52
control Na excretion via hormones: RAAS- renin release signal to jux cells mediated by? and wat is released by macula densa cells
- mediated by paracrines NO | - prostaglandin E2 released by macula densa cells
53
function of RAAS hormones regulation of Na balance: Angiotensin II
- increase release of steroid hormone, aldosterone (adrenal cortex) - increase thirst - release ADH
54
aldosterone function: and effect
- stimulates NaCl reabsorption in distal tubule, cortical collecting duct - decreased Na excretion for more +ve Na balance (more in than out) = increase ECF vol (water follows Na) - increase BP
55
aldosterone: without it ?
- need a v high Na diet to prevent death by circulatory collapse due to Na depletion - Addison's crisis: acute - Addison's disease: chronic
56
aldosterone: mechanism
- is steroid hormone will cross BASOlateral mem - binding to receptor of nuclear mem - hormone + receptor complex regulates transcription of mRNA promoting (increase) production of LUMINAL Na and K channel proteins, enzymes for ATP synthesis (mitochondria) and BASOlateral Na/K exchange pump proteins
57
ANP: main job
- decrease reabsorption of Na in collecting duct by
58
ANP: decreases reabsorption of Na by (4)
- closing LUMINAL Na channels - inhibiting Na/K pump - inhibiting release of renin/ aldosterone - inhibiting ADH release
59
control Na excretion via nerves: changes in plasma/ECF detected by/ transmitted to
- atrial vol receptors | - transmitted to NTS
60
control Na excretion via nerves: sensory input received from ? monitor
- input from renal mechanoreceptors | - monitor renal aa, venous, urethral P, renal chemoreceptors
61
control Na excretion via nerves: afferents from kidney impact
- paraventricular nucleus (PVN) in hypothalamus
62
control Na excretion via nerves: incoming info from PVN + NTS prod.?
- produces apparent appropriate lvl of activation in RVLM
63
control Na excretion via nerves: wat signals arise from RVLM and transmitted
- peripheral eff signals arise | - transmitted via pre/post ganglionic neurons travelling in renal nn
64
control Na excretion via nerves: symp output to kidney increased
- when ECF vol falls | - cause increased Na reabsorption, decreased Na excretion
65
control Na excretion via nerves: increase symp input to renal nn- (3)
- increase renin release (jux ap: ß adrenergic receptors) - decrease GFR causing vasorestriction in aff (more pronounced) and eff arterioles (å adrenergic receptors on smooth mm cells) - increase NaCl reabsorption directly from tubular cells mainly in proximal tubule (å adrenergic receptors on tubular epithelial cells)
66
what systems increase/decrease total body Na content, and BP (3)
- RAAS - ANP - symp nn
67
if BP low: increase/decrease?
increase: renin, RAAS, symp stimulation decrease: ANP lvl
68
inability of pressure natriuresis/diuresis sys to return BP to set point after maintained salt intake: RAAS sys effect
- shift excretion curve so equilibrium point falls at normal BP
69
inability of pressure natriuresis/diuresis sys to return BP to set point after maintained salt intake: if salt intake rises, wat falls?
- renin, angiotensin II and aldosterone fall | - allow excretion at lower BP, shifting curve to L

5. ADV PHYS (10 decks)

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