renal 2 Flashcards
Describe the myogenic mechanism of autoregulation
- Controls Renal blood flow and Glomerular filtration rate
- when the tension on the walls of vessels increase –> contraction of smooth muscle to raise vascular resistance –> prevents excessive RBF and GFR
What is the usual relationship in the regulation of GFR and RBF
- they are regulated in parallel as arterial pressure increases (consistency); GFR is even more heavily controlled
what substance is not very well controlled with an increase in arterial pressure
URINE OUTPUT
Describe the method of TUBULOGLOMERULAR feedback for autoregulation during increasing arterial pressure
- If you increase renal arterial pressure –> increase GFR and RBF, so need to feedback to decrease them
- Solution = CONSTRICT the AFFERENT arterioles
Describe autoregulation for increased renal arterial pressure (2 overall effects)
- Increase renal Arterial pressure, increase GFR and RBF –> less time to reabsorb water, get large volume at loop of henle –> also less NaCl removed so more reaches macula densa –> increased intake of NaCl to macula densa –> increase release of ATP and adenosine to smooth muscle –> increased intracellular Ca2+ –> increase vasoconstriction of AFFERENT ARTERIOLE (vasodilation would increase the GFR and RBF)
What do the ATP and adenosine also do in the kidney
inhibit release of renin
What about a tubuloglomerular feedback mechanism for DECREASED renal arterial BP
renal BP falls –> GFR decreases –> NaCl in tubule FALLS –> UPTAKE NaCl from macula densa –> decreases adensoine and ATP –> VASODILATE the afferent arteriole –> GFR increased and release of renin (so more angiotension II to constrict the efferent to further assist)
How do we maintain Na concentration
Make a gradient with the Na/K ATPase so sodium can always flow down conc gradient into blood from the tubular fluid
what are the 4 overal reasons for autoregulation
1) many activities change BP, but don’t necessarily want to tie these to GFR or RBF
2) BP changes suddenly, but don’t want interference with urine
3) hypertension could damage glomerulus
4) NE is released with symp nervous stimulation which interferes with autoreg. (afferents constrict and GFR lessens but we want opposite for instance)
What are the relationships of hypertension to renal disease
- cyclic; Hypertension causes renal damage, but any renal damage also causes more hypertension
describe the vasodilator prostaglandins
- PGE2 and PGI2 (prostacyclin)
- prostacyclins are vasodilators to oppose things like NE; become unapposed vasoconstriction and renal damage when PGE2 and PGI2 are reduced.
What are the effects of NSAIDS on the prostacyclins/prostaglandins
NSAIDS inhibit prostoglandin synthesis and cause ISCHEMIC RENAL DAMAGE (b/c of unhibited vasoconstriction)
define chronic renal disease
- if # of nephrons goes down, each nephron just works harder to maintain GFR; do this by increasing PGE2 and PGI2 –> dilate afferent arterioles and increase single nephron GFR
What if the patient who is compensating for chronic renal disease takes NSAIDS
- no more prostaglandins, can get immediate renal failure
which blood flow in kidney is especially dependent on prostaglandins
medullary
what is the first sign of NSAID OD and the first sign of NSAID abuse
- NSAID O.D. = medullary ischemic injury
- NSAID Abuse = loss of ability to concentrate urine
What does renin-angiotensin cycle control
BP and salt
- also cordinates cardio, renal, hypothalamic (thirst and ADH/vasopressin), and ANP hormone
describe Natriuretic peptide
- atrial and brain natriuretic peptides (ANP and BNP)
- relax afferent arteriole so increases (GFR
- Inhibit release of renin
- inhibit angiotensin II
- Stops Na reabsorb in med. coll. duct
describe erythropoietin.
- mostly in the kidney
- reason why kidney disease results in anemia
- STIMULATED BY lack of O2 (hypoxia!!!)
How does erythropoietin play into the grand scheme of kidney
- Anemia and hypoxia are decreasing O2 so this tells kidney to produce MORE erythropoietin, thus trying to fix the problem
- Polycythemia is increasing erythrocyte mass so erythropoietin production is DECREASED
What is the Vit D we actually take in within our diet and what happens to it
Vitamin D is taken in by skin or diet and transformed into 14-hydroxycholecaliferol in liver and then 1,25-dihydroxy Vit D in kidney
- prohormone
What does 1,25-dihydroxy Vit D do for the body
- Increase absorption of Ca2+ and P and stimulates renal tubules to reuptake the Ca and P
what does PTH do
Control levels of plasma Ca2+ (calcium acts directly on parathyroid; increases Ca and decreases PTH)
What are teh actions of PTH
1) stimulates activation of Vit D in kidney
2) increase renal tubule Ca reabsorptions
3) reduces phosphorus proximal tubule reabsoprtion (increases P in urine)
4) increases movement of Ca from bone
What are the actions of CALCITONIN
- THYROID C cells release calcitonin in response to HYPERCALCEMIA
- Lowers Ca2+ in blood via stimulate bone formation
what is the official definition of chronic renal failure
- LOW GFR that results in high phosphate in plasma (decreased excretion), elevated PTH, increase bone resorption, and renal osteodystrophy
what would the elevated PTH try to do
- increase activation of Vit D
- if not enough kidney cells, you can’t SO decrease in calcium absorbed from intestine
- this causes less Calcium in plasma so increase in PTH secretion; WEAK BONES!!!
what are the effects of angiotensin II
- vasoCONSTRICTION of vascular smooth muscles
- increases aldosterone secretion in adrenal cortex
- increases symapthetic tone in CNS
- increaes releases of ADH in CNS
- Increases thirst in CNS
- Primarily CONSTRICTS Efferent arteriole (raise GFR)
- Increases proximal tubule sodium reabsorption through upregulation of Na/H transporter
describe fibroblast growth factor 23 (FGF 23)
- FGF23 production stimualted by Vit D hormone (calcitriol) and elevated P.
- it is a peptide hormoen created by osteoblasts and osteocytes
- FGF 23 DECREASES the reabsorption of P in kidney and decreases production of calcitriol (opposite of PTH)
What are the effects of contricting the Efferent arteriole on RBF and GFR
- GFR increases and RBF decreases
what are the effects of constricting the afferent arteriole on RBF and GFR
- GFR decreases and RBF decreases
what is the result of dilating both efferent and afferent arterioles
- increases glomerular hydrostatic pressure by vasodilating both efferent and afferent
