Exam3Lec5RenalHormones/ControlofBodyWaterandSalt Flashcards
Explain red blood cell production with low O2 delivery
- Low O2 delivery: hypoxia or ischemia
- Leads to an accumulation of hypoxia 1α (↑HIF-1α) in tubular intertitial cells
- This triggeres the synthesis and release of Erythropoietin (Epoetin-α)
- Epoetin-α goes to bone barrow for rbc production (Erythroid Precursor Cells to normoblasts)
Erythropoietin comes from interstitial cells of kidney
maturation of erythopoietycytes is controlled by Erythropoietin (Epoetin-α)
What is the difference between HIF-1α under normoxia and hypoxia
In normoxia: HIF-1α is degraded
In hypoxia: active HIF dimrer is produced and this leads to erythropoiesis
What does renin regulate?
blood pressure and sodium output
What is renin secreted by?
Juxtaglomerular cells (JG cells)
smc has lots of renin
What 3 mechanisms trigger renin secretion?
- low blood pressure activates renal vascular receptor (baroreceptor inside kidney) and incr renin release from JG cells
- low blood pressure also decr GFR and delivery of Cl- to Macula Densa in the distal tubule which incr renin from JG cells
- low blood pressure causes a reflex activation of renal sympathetic nerves which incr renin release from JG cells.
all mechanisms are triggered by low BP
note macula densa has 2 fxns: sensory for renin release when BP decr and sensor for JG cells to maintain aff arteriole resistance (tubular feedback)
Is Angiotensin 2 a powerful vasodilator or constrictor?
Powerful vassoconstrictor, thats why BP can incr
When BP decr, fill in what occurs
A 48-year-old 60 Kg woman is seen in a clinic for her progressive uncontrollable hypertension. During the past year she has been treated with combinations of the following drugs with only partial success: a beta-receptor blocker, an alpha-receptor blocker, a calcium channel blocker, and several different diuretics. Blood pressure was 200/110 mmHg while on medications. The patient was then taken off other medications and treated with an angiotensin converting enzyme (ACE) inhibitor for two days. This drug lowered her blood pressure to 130/82 mmHg but caused her kidney function to further deteriorate. She eventually (following several other tests) received a right renal artery bypass graft, which normalized her blood pressure and kidney function.
What is the rationale for each of the drugs tried initially in this patient?
(a): beta receptor blocker: decr renin release (less fluid retention), and decr hr force
(b): alpha receptor blocker: vasodilates bv
(c): calcium channel bloker: relaxes sm
(d): dieuretics: excretion of Na+
A 48-year-old 60 Kg woman is seen in a clinic for her progressive uncontrollable hypertension. During the past year she has been treated with combinations of the following drugs with only partial success: a beta-receptor blocker, an alpha-receptor blocker, a calcium channel blocker, and several different diuretics. Blood pressure was 200/110 mmHg while on medications. The patient was then taken off other medications and treated with an angiotensin converting enzyme (ACE) inhibitor for two days. This drug lowered her blood pressure to 130/82 mmHg but caused her kidney function to further deteriorate. She eventually (following several other tests) received a right renal artery bypass graft, which normalized her blood pressure and kidney function.
2) Why did the ACE inhibitor lower her blood pressure?
this pathway is inhibited
A 48-year-old 60 Kg woman is seen in a clinic for her progressive uncontrollable hypertension. During the past year she has been treated with combinations of the following drugs with only partial success: a beta-receptor blocker, an alpha-receptor blocker, a calcium channel blocker, and several different diuretics. Blood pressure was 200/110 mmHg while on medications. The patient was then taken off other medications and treated with an angiotensin converting enzyme (ACE) inhibitor for two days. This drug lowered her blood pressure to 130/82 mmHg but caused her kidney function to further deteriorate. She eventually (following several other tests) received a right renal artery bypass graft, which normalized her blood pressure and kidney function
3) Why did the ACE inhibitor exacerbate her kidney problem?
might have this answer wrong
Her 2 kidneys responds differently.
1. One kidney has renal stenosis (narrow arteriole) , so it cannot “see HTN” it sees HYPOtension. This leads to renin release, activating RAAS system to incr BP.
2. The other kidney is normal and it “sees HTN” so it senses high perfusion pressure. It adapts by Incr RAAS RESISTANCE to maintain GFR.
review this ***kidney in stenosis: ACE inhibitor leads to decr Ang2 leading to decr GFR (b/c FF decr). With no ANG2 VC activity, efferent arteriole is not VC to incr GFR
How do renal prostaglandins respond to low blood pressure?
It responds to excessive vasoconstricction so it vasodilates
Explain what occurs with a decr in BP
What two isoforms of prostaglanfdins are major renal Vasodialotors for
PGE2 and PGI2
What is vioxx?
is a cyclooxygenase-2 (COX-2) inhibitor, and was recalled in 2004 because of increased risk of cardiovascular problems (because can’t vaso dialate)
What factors are the body trying to
control in order to control body salt and water?
ECF volume and ECF osmolality
How can our body control water?
By controlling water intake and by controlling water output
Control of water intake is by thirst. What drives thirst?
Stimuli of thirst
- Increased Osmolality
- Decreased Arterial Pressure
- Decreased Blood Volume
- Angiotensin II
these all relate to ECF osmolality and ECF volume
How do we control water output?
By ADH secretion
What triggeres ADH secretion
stimuli of ADH secretion
1) Increased Osmolality
2) Decreased Arterial Pressure
3) Decreased Blood Volume
4) Angiotensin II
5) Trauma
6) Surgery
7) Drugs eg. opiates and anesthetics.
1-3 are all related to ECF osmolaloty and volume
What occurs to the following when there is an incr in plasma osmolality or decr in BP?
leads to an incr in thirst and incr in ADH
both leads to an incr in water retention in order to decr plasma osmolality and incr BP
Explain what is occuring in area 1 and area 2
- Area 1: Area b/w the two curves is sodium retention, Intake is incr but you are not excreting Na+ fast enough. The body is accumlating lots of Na+ and this leads to water reabsoprtion. Water reabsoprtion leads to weight gain
- Area 2: Area b/w the two curves is sodium deficit. Intake is decr but you are excreting Na+ too fast. The body has little Na+ and you are excreting more H20. Excretion of H20 leads to weight loss.
Regulation os Na+ excretion
Fill in what occurs with an Incr in NaCl intake
Fill in what occurs with Hemorrhage (lost blood)
What does this shift represent?
Adrenal insufficiency
(cannot make enough aldosterone so you cannot reabsorb a lot of Na+-> you loose lots of Na+, hence ECF)
What does this shift represent?
SIADH (syndrome of inappropriate antodiuretic hormone-> lots of ADH so you keep reabsorbing water)
