renal physiology Flashcards
what are the two capillary beds of the renal circulation
- glomerular
- peritubular
how are the renal capillary beds arranged and how are they separated
arranged in series, separated by the efferent arteriole -> helps to maintain pressure in both beds
what is the normal filtration rate of the kidney
180L/day
how much water is excreted via urine a day
1.5L
what is the solute conc in urine
600 miliosmoles
3 fundamental functions of the kidney
- filtration
- regulation (BP, electrolytes, Acid base etc.)
- production + activation of key hormones (erythrocytosis, etc.)
what are the 6 overarching effects the kidney has
- volume regualtion
- concentration
- pH
- metabolic
- excretory
- endocrine
how is volume regulated by the kidneys
directly through excretion/retention of fluid -> this results in BP control
what is the metabolic function of the kidney (2)
- gluconeogenesis -> usually immesuarable amounts but when fasting can produce a lot of glucose
- Vit D activation (CaPO4 metabolism)
endocrine functions of the kidney (3)
- RAAS -> produced renin
- EPO - erythrogenesis
- vit D control
why must blood flow be controlled in the renal system (2)
- blood flow is related to the function of the kidney (filtration + excretion) so must be maintained
- in order to protect the delicate arteries of the renal system -> autoregulation
what is the main purpose of blood flow in the kidney
to supply enough plasma to govern rate of filtration needed for bodily fluid volume and solute control
what is GFR determined by
net filtration pressure across the glomerular capillaries
what is glomerular blood flow directly proporitonal to
changes in pressure
what are the 2 major sites of resistance control in the kidney vascular bed
afferent and efferent ARTERIOLES
how is control of blood flow, hydrostatic pressure and filtration maintained by the arterioles
selective vasoconstriction and dilation of the afferent and efferent arterioles results in highly sensitive control of blood flow etc.
how does increased Afferent resistance change renal blood flow and net ultrafiltration pressure
RBF - decreased
NFP - decreased
how does decreased Afferent resistance change renal blood flow and net ultrafiltration pressure
RBF - increased
NFP - increased
how does increased Efferent resistance change renal blood flow and net ultrafiltration pressure
RBF - decreased
NFP - increased
how does decreased Efferent resistance change renal blood flow and net ultrafiltration pressure
RBF - increased
NFP - decreased
what are the key mediators for renal blood flow (6)
vasoconstrictors
1. sympathetic nerves
2. angiotensin II
vasodilators
3. prostoglandins
4. natriuretic peptides
5. nitric oxide
6. bradykinin
how do sympathetic nerve influence renal blood flow
- release NA into the intersititial space in response to low fluid volume/fight or flight response
- high levels of NA causes vasoconstriciton of both afferent and efferent arterioles
- decrease in blood flow
- reduced fluid loss
how does angiotensin II influence renal blood flow
causes vasoconstriction of the afferent and efferent arterioles in response to low extracellular volume
what other mediator does angiotensin II work alongside
prostoglandins -> ultimately results in efferent constriction > afferent thus maintaining GFR when renal perfusion is reduced
how do prostaglandins influence renal blood flow
- dampen the effect of vasocontrictors but causing dilation of the afferent arteriole
- cause vasodilation to prevent harmful vasoconstriciton and renal ischaemia
how do natiuretic peptides influence renal blood flow
released from the heart in response to increased pressure and effective circulating volume -> causes vasodilation of the arterioles -> increased blood flow and GFR
ANP also inhibits the secretion of renin => less angiotensin II
what are the 2 main natriuretic peptides
BNP; ANP
what is the purpose of renal autoregulation
to maintain bloodflow and GFR within narrow limits despite changes in mean arterial pressure (changes between 60-100 mmHg)
what are the 2 basic mechanism of renal autoregualtion
- myogenic response of smooth muscle of afferent arterioles
- tubuloglomerular feedback mechanism
what is the myogenic response in renal autoregulaton
the inherent ability of the blood vessels to respond to changes in vessel circumference by constricting/relaxing
-> constriction in response to increased pressure prevents the vessel from being overstretched and also increases vascular resisitance to prevent excessive increase in renal blood flow and GFR when BP rises
venturi effect
what is the bayliss effect
describes the reaction of smooth muscle cells in the arterial wall to changes in blood pressure
how does the tubuloglomerular mechanism of renal autoregulation work (8)
- increased GFR
- flow through proximal tubule increases
- flow past macula densa increases
- in response to increased NaCl detection, the macula densa sens paracrine signals to the afferent arteriole
- afferent arteriole constricts
- resistance in afferent arteriole increases
- hydrostatic presure in glomerulus decreases
- GFR decreases
what is the renal corpuscle made up of
- glomeralus
- bowman’s capsule
are there arteries and veins in the renal corpuscle
no, only arterioles
what is the glomerular filtrate
the blood that enters the glomerulus to be filtered via the ultrafiltration barrier
above what size molecules are filtered out the capsules in ultrafiltration (i.e what size can pass through)
<1.8 nM
what are the 3 layers of the ultrafiltration barrier and what do they allow to pass through
- fenstrated capillaries - allows anything except for blood cells to pass through
- basement membrane - prevents filtration of large proteins
- podocytes - part of the bowmans capsule, only allows small molecules to pass through
apart from the filtration layers, how else is the ultarfiltration barrier molecule selective
it is charge selective -> the layers contain-vely charged glycoprotiens which makes it hard for polar molecules e.g. albumin to pass through even if they are within the size range
what is hydrostatic pressure
the force exerted by a fluid on the walls of its comprtment
what is oncotic pressure
the pressure exerted by plasma proteins (most notibly albumin) -> pulls water back into the capillary
what forces oppose the hydrostatic pressure of the glomerular filtrate
the oncotic pressure of the filtrate (only minute as not many proteins in the glomerular filtrate) and the hydrostatic pressure of the bowman’s capsule
what is the renal net filtration pressure equation
NFP = glomerular hydrostatic pressure - (bowmans capsule hydrostatic pressure + glomerular oncotic ressure)
what is GFR
glomerular filtration rate - the total filtrate produced by ALL renal corpuscles in BOTH kidneys in 1 min
what factors does the GFR take into account (3)
- NFP
- SA available for filtration
- prermeability of the glomerulus
how can GFR change
change in filtration coefficent or NFP
what is the MOA of ADH
- ADH release begins when plasma osmolarity is <280 mOS/L
- ADH acts on the distal convoluted tubule and collecting duct to increase water reabsorption independent of sodium
- ADH stimulates the insertion of aquaporin-2 channels onto the luminal membrane, allowing the free entry of water
- ADH also causes vasoconstriction of arterioles
-> water is retained
