Autoregulation YT Flashcards
(18 cards)
What is renal autoregulation
Ability for kidney to modify blood flow and therefore control amount of urine made
What are the two intrinsic autoregulation mechanisms?
Myogenic mechanism
Tubuloglomerular feedback mechanism
What are the extrinsic mechanism
Really kick in when bp is low
Sympathetic nervous system
RAA (A)S system renin, angiotensin, aldosterone, (ADH) system
High BP causes
Higher glomerular hydrostatic pressure
increase in glomerular filtration rate
How does the kidney prevent damage from high bp?
High BP causes stretching on arteriole- Stretch mediated sodium channels open, causing stimulus to sarcoplasmic reticulum
Lots of calcium released-increases contraction of the smooth muscle
Low GBF causes lower GFR (autoregulatory system)
Low BP?
Reduced contraction, more relaxation of arteriole muscle, allowing more to flow through
Increases glomerular blood flow
increases GFR
Tubuloglomerular feedback
Macula densa cells detect the concentration of ions in the blood, and if the ion concentration is too high in the DCT, releases adenosine afferent arteriole
The opposite also applies when ion levels are too low, except PGI2 and NO is released, acting on the afferent arteriole
Adenosine: causes vasoconstriction of afferent arteriole, lower GFR, less filtration, less ions filtered (sodium chloride)
PGI2 +NO : Vasodilation, GFR increase, more filtration
What does adenosine act on when bp is high
Juxtaglomerular cells- adenosine inhibits renin release
What is the effect of PGI2 and NO on juxtoglomerular cells?
Stimulates renin release
activates RAAS when low BP
Sympathetic Nervous System (extrinsic mechanism) (low blood pressure)
Baroreceptors in the carotid arteries
Sends signal to brain stem, particularly medulla oblongata
ramps up sympathetic nerve response
Low BP can cause
kidney injury
What can sympathetic nerve response do in low BP
1) releases epinephrine and norepinephrine- increases heart rate to increase BP
2) Increase stroke volume of the heart
Both increases the BP
Low BP can cause vasoconstriction through
Activation of the Alpha receptors on the afferent receptor, causing vasoconstriction to get blood flow to other organs
Triggers renin release leading to RAAS system
RAA(A)S in Low BP
Juxtaglomerular cell in afferent arteriole releases Renin
Angiotensinogen produced by liver is cleaved (broken) turning into angiotensin I
Angiotensin I then moves to capillary in lung, where ACE converts it into angiotensin II
What does angiotensin II do?
1)Stimulates hypothalamus—>posterior pituitary to release ADH (this stimulates thirst response)
2)Acts on adrenal cortex (zona glomerulosa) triggers aldosterone release (acts on DCT) increasing water and sodium: increasing blood volume+ blood pressure
3)Kidneys; bind to receptors on efferent receptors causing vasoconstriction-forcing a back up, more blood stays in the glomerulus, so more filtered out, increased GFR
4) Causes cells in PCT to reabsorb more sodium and water, increasing blood volume, increasing blood pressure.
Atrial natriuretic peptide (released in high BP)
Blocks RAAS system
Encourages natriuresis-sodium and water excretion
Lowers blood pressure, lowers blood volume
Kidney injury due to hypertension
In the kidneys, as a result of benign arterial hypertension, hyaline ( pink, amorphous, homogeneous material) accumulates in the wall of small arteries and arterioles, producing the thickening of their walls and the narrowing of the lumina- hyaline arteriolosclerosis. Consequent ischemia will produce tubular atrophy, interstitial fibrosis, glomerular alterations ( smaller glomeruli with different degrees of hyalinisation- from mild sclerosis of glomeruli) and periglomerular fibrosis. In advanced stages, renal failure will occur
Chicken and egg scenario
Kidney injury can lead to hypertension due to impaired regulation of sodium and water excretion and excessive renin production, especially in vascular injury.
Conversely, chronic hypertension can lead to kidney damage by causing capillary injury and fibrosis in the glomeruli and interstitium.