5.1 renal blood pressure Flashcards
What’s the difference between what the intracellular and extracellular compartments consist of ?
intracellular = fluid contained within all the body cells
extracellular = all the fluids outside the cells, including fluid in the interstitial (tissue) spaces and in the intravascular space (blood vessels)
Too much interstitial fluid results in ..1… in the following 3 locations: …2..
- oedema
- ankles , lower back, abdomen
where is most blood contained within ?
veins
“For a given level of ..1.., the ‘fullness of the ..2…’ and the rate of ..3… vary directly with the ..4..”
- vascular capacity
- circulation
- venous return
- volume of blood
effect of circulating volume on venous pressure ?
directly related so :
CV INC = VP INC or CV DEC = VP DEC
What is equation for frank-starling’s law ?
CO = SV x HR (where SV = EDV - ESV)
CO = cardiac output
SV = stroke volume
HR = heart rate
EDV = end diastolic volume
ESV = end systolic volume
i.e. more in -> more out , VP INC will INC CO
Equation for mean arterial pressure
CO x TPR
CO = cardiac output
TPR = total peripheral resistance
At constant TPR what happens to CO ?
INC CO which would INC AP
but tissue demand for blood flow not increased
tissues autoregulate blood flow by INC peripheral resistance
this further INC AP
What is BP influenced by ?
- cardiac factors
- peripheral resistance
- blood volume
- viscosity
- arterial elasticity
What do kidneys require to maintain GFR ?
a stable mean arterial blood pressure so BP must not be too high nor too low
approx. what value must GFR be to maintain renal function and prevent renal damage (remain constant value) ?
120 ml/min/1.73 m^2
GFR is maintained by .1… through the ..2.. arterioles, but only within limits (mean arterial pressures of ..3.. mmHg).
- autoregulation
- afferent and efferent
- 80-180
How is blood pressure regulated short-term ? [don’t understand this !]
autonomic regulation - baroreceptor reflex - respond to vascular stretch
* adjust to sympathetic input to peripheral resistance vessels to alter TPR
* adjust sympathetic and parasympathetic inputs to the heart, to alter CO
Short-term BP control is ..1.. on long-term BP control
1 = superimposed
Long-term BP regulation is:
1. determined by ?
2. ECF volume is primarily determined by ?
3. kidneys primarily control long-term BP by controlling ?
- ECF volume
- total amount of osmotically-active solute within the ECF
- the amount of Na+ in the ECF
Na+ and Cl- comprise >..1…% of osmotically-active solutes in the ECF.
Movement of Cl- is mostly …2… to movement of Na+.
The amount of Na+ in the ECF is, therefore, the ..3.. of ECF volume.
..4.. in the kidneys is therefore the primary determinant of ECF volume and long-term BP regulation.
- 90
- secondary
- primary determinant
- Na+ reabsorption
WHO recommended limit of sodium/ day ?
2g
What’s difference between obligatory and variable reabsorption of Na+ ?
% of Na+ reabsorbed or excreted through renal system
PCT - 65% reabsorbed
LoH - 25% reabsorbed
distal tubule - 8% reabsorbed
outer med CD - 3% reabsorbed
urine - 0.4% excreted
Na+ reabsorption (from the tubular fluid to the blood) dilutes the tubular fluid as it moves along the tubule.
The TAL of the Loop of Henle is the ‘ ..1… segment’. Reabsorption in the ..2… is control dependent.
- Diluting
- DT + CT
How many g of Na is ingested per day ?
10
what maintains TAL Na+/K+/2Cl- co-transporter activity ?
It dilutes the tubular fluid by moving Na+/K+/2Cl- into the tubular epithelium of the TAL
K+ ions then diffuse back via the ROMK into the tubular lumen to maintain the co-transporter activity
What allows paracellular reabsorption of Na+, Ca2+ and Mg2+ from the TAL ?
return of K+ maintains a +ve charge in the TAL lumen
What do loop diuretics block ? give an example of one
- blockst he Na+/K+/2Cl- co-transporter by competing for Cl-
- furosemide
DCT
Connecting tubule and collecting ducts
What sensors are involved in regulating ECF volume ?
- juxtaglomerular apparatus - granular cells of JGA release renin in response to low BP initiating RAAS
- atria - released natriuretic peptides to promote Na+ excretion
- carotid sinus - regulates activity of sympathetic nervous system , relayes hypovolemic stiumlus to vasopressin
effector mechanisms of volume regulation respond by doing what ?
altering Na+ excretion and systemic vascular resistance
What stiumlates renin secretion ?
Low BP (sensed by cardiopulmonary baroreceptors) triggers sympathetic stimulation and catecholamine release to stimulate β1 receptors in the JGA
Low BP (sensed by afferent arteriole baroreceptors) stimulates local release of prostaglandins
Increased sympathetic activity via renal nerves
What inhibits renin secretion ?
Increased Na+/Cl- reabsorption by the macula densa cells of the early distal tubule
Elevated BP in the afferent arteriole
Angiotensin II (Negative-Feedback)
Vasopressin
How does angiotensin II reverse low bP caused by hypovolaemia ?
- Arteriolar vasoconstriction to ↑ systemic BP
- Directly stimulating Na+ reabsorption to ↑ circulating volume and ↑ BP
- Indirectly stimulating Na+ reabsorption by stimulating the release of aldosterone from the adrenal cortex.
Aldosterone …
If blood pressure decreases ?
Aldosterone stimulates expression of ENaC channels in the principal cells to allow
Na+ reabsorption from the connecting tubules/collecting ducts to ↑ ECF volume and ↑ BP
if blood pressure increases ?
Atrial Natriuretic
Peptide (ANP) inhibits expression of ENaC channels in the principal cells. This reduces
Na+ reabsorption from the connecting tubules/collecting ducts, causing ↓ ECF volume and ↓ BP
