Lecture 5: Renal Hormones/Control of Body Water and Salt 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 interstitial cells
- This triggers the synthesis and release of Erythropoietin (Epoetin-α)
- Epoetin-α goes to bone barrow for RBC production (Erythroid Precursor Cells to normoblasts)
Review Slide 3
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 dimer is produced and this leads to erythropoiesis (creation of RBC)
What does renin regulate?
blood pressure and sodium output
What is renin secreted by?
Juxtaglomerular cells (JG cells)
SMC has lots of renin
List the 3 mechanisms that trigger renin secretion?
- ↓ blood pressure activates renal vascular receptor (baroreceptor inside kidney) and ↑ renin release from JG cells
-
↓ blood pressure also ↓ GFR and delivery of Cl- to Macula Densa in the distal tubule which ↑ renin from JG cells
3.↓ blood pressure causes a reflex activation of renal sympathetic nerves which ↑ renin release from JG cells.
all mechanisms are triggered by low BP
Is Angiotensin 2 a powerful vasodilator or constrictor?
Powerful vassoconstrictor, that’s why BP increases when it’s present
When BP decreases explain the effects of the Renin-Angiotension-Aldosterone System on factors listed below
- Renin (kidney)
- Angiotensin I
- Angiotensin II
- ADH & Thrist
- FF
- Aldosterone
- Na+ Reabsorption
- ↑ Renin (kidney)
- ↑ Angiotensin I
- ↑ Angiotensin II (vasoconstriction)
- ↑ ADH & Thirst (water reabsorption)
- ↑ FF (oncotic pressure)
- ↑ Aldosterone
- ↑ Na+ Reabsorption
Review Slide 10
Review Slide 10
How do renal prostaglandins respond to low blood pressure?
It responds to excessive vasoconstriction, so renal prostaglandins vasodilates
Review Slide 13
What two isoforms of prostaglandins are major renal Vasodilators?
PGE2 and PGI2 (in response to ↓ RBF)
What is Vioxx?
is a cyclooxygenase-2 (COX-2) inhibitor, and was recalled in 2004 because of increased risk of cardiovascular problems
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 (intake=output)
Fluid: primary driver of intake, Urine: primary driver of output
Control of water intake is by thirst. What drives thirst? (4)
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 triggers ADH secretion? (7)
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 Thirst and ADH secretion when there is an increase in plasma osmolality or decrease in BP?
- Leads to an increase in thirst and increase in ADH secretion
- Both leads to an increase in water retention in order to decrease plasma osmolality and increase BP
Explain what is occuring in Area 1 and Area 2 in the image below
- Area 1: Area b/w the two curves is sodium retention, Intake is increase 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 decreased but you are excreting Na+ too fast. The body has little Na+ and you are excreting more H2O. Excretion of H2O leads to weight loss.
Regulation of Na+ Excretion
What occurs to the mechanisms listed below with an Increase in NaCl Intake
- Blood Volume
- Atrial Pressure
- Arterial Pressure
- Plasma Protein
- ANP Secretion
- GFR
- Sympathetics
- Renin
- Angiotensin II
- Aldosterone
- Na+ Excretion
Either increases or decreases
HIGH yield
- ↑ Blood Volume
- ↑ Atrial Pressure
- ↑ Arterial Pressure
- ↓ Plasma Protein
- ↑ ANP Secretion
- ↑ GFR
- ↓ Sympathetics
- ↓ Renin
- ↓ Angiotensin II
- ↓ Aldosterone
- ↑ Na+ Excretion (aka ↓ Na+ reabsorption)
What occurs to the mechanisms listed below when Hemorrhage occurs
- Blood Volume
- Atrial Pressure
- Arterial Pressure
- ANP Secretion
- GFR
- Sympathetics
- Renin
- Angiotensin II
- Aldosterone
- ADH
- H2O Excretion
- Na+ Excretion
Either increases or decreases
HIGH yield
Hemorrhage-loss of blood
- ↓ Blood Volume
- ↓ Atrial Pressure
- ↓ Arterial Pressure
- ↓ ANP Secretion
- ↓ GFR
- ↑ Sympathetics
- ↑ Renin
- ↑ Angiotensin II
- ↑ Aldosterone
- ↑ ADH
- ↓ H2O Excretion
- ↓ Na+ Excretion (aka ↑ Na+ reabsorption)
What does this D-Y graph shift represent?
- Adrenal insufficiency
- (cannot make enough aldosterone so you cannot reabsorb a lot of Na+-> you lose lots of Na+, hence ECF gets smaller)
What does this D-Y graph shift represent?
SIADH (syndrome of inappropriate antidiuretic hormone-> lots of ADH so you keep reabsorbing water)
What does this D-Y graph shift represent?
Infusion of isotonic NaCl ( Na+ and Cl- both go to the ECF compartment that is why it’s volume is raised)
What does this D-Y graph shift represent?
High NaCl Intake
