Renal System 5 Renin A2 aldosteron Flashcards
What is one of the main functions of juxtaglomerular cells (JG)?
Release of Renin
What are the 3 stimuli that stimulate the release of Renin?
1) Sympathetic NS
2) Less stretch on afferent arteriole due to less blood pressure and less blood flow -> JG is less stretched -> release of Renin
3) Signal from Macula Densa: when rate of Na Cl in Macula Densa slows down -> signal to JG to release Renin
What are the 3 stimuli that stimulate the release of Renin?
1) Sympathetic NS
2) Less stretch on afferent arteriole due to less blood pressure and less blood flow -> JG is less stretched -> release of Renin
3) Signal from Macula Densa: when rate of Na Cl in Macula Densa slows down -> signal to JG to release Renin
What are the effects of sodium and H2O loss in diarrhea?
Plasma volume down -> Venous pressure down
Venous pressure down -> Venous return down -> Atrial pressure down
Atrial pressure down -> ventricular EDV down -> SV (stroke volume) down -> CO down -> Arterial blood pressure down
The sum effect of Na+ and H2O loss in diarrhea?
Sum: Venous, atrial, and arterial pressure goes down -> causing activity of renal sympathetic nerves
What effect do Na and H20 loss have on the kidney?
-Activity of renal sympathetic nerve causes constriction of afferent renal arterioles, causing reduced blood flow -> drop in net glomerular filtration pressure
-Arterial pressure causing the net glomerular filtration pressure to drop directly
BOTH: causing drop in GFR -> Na+ and H2O ecxretion is reduced
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Overall effect of Na+ and H2O loss?
Drop in GFR -> Drop in Na and water excretion
Because of increased loss, more of them should be kept by decreasing pressure glomerular capillaries -> reduce of GFR
How is renin involved in Na and H2O loss?
-Reduction of pressure is a stimulus (less stretch of JG) to release Renin
-Reduced GFR will slow down the appearance of Na+ and Cl in the Macula Densa -> stimulate the JG to release Renin
How does Renin work?
Renin released in the kidneys is an enzyme converting Angiotensinogen (always present in the bloodstream produced in the liver) to Angiotensin I
What happens to Angiotensin I?
It gets converted to Angiotensin II by Angiotensin-converting enzyme (ACE I present in endothelial cells of lungs and kidneys)
What are the effects of Angiotensin II?
-Cardiovascular system: Vasoconstriction -> increase blood pressure (Homeostatic -> more blood flow will stretch JG -> renin stops)
-stimulates Adrenal cortex to secrete aldosterone -> promotes salt and water retention
What do water and H2O retention look like?
more reabsorption and less excretion of water and Na+
How does aldosterone work?
EXAM !!!
Aldosterone (lipophilic) walks through the membrane of principal cells -> and acts as a transcription factor
1) for Na+ channel: more Na reabsorption from the urine back to the blood
2) for proteins responsible for the TCA cycle to produce more ATP, ATP is needed for the Na-K ATPase to pump Na back into the blood
Different functions of Angiotensin II:
-direct Vasostrictor: activating vascular smooth muscles -> increases BP
-stimulates aldosterone release: Na+ and water retention -> increases BP
-stimulates vasopressin release -> increase water retention -> increase BP
-stimulates thirst: increase water intake -> increase BP
What is a natriuretic effect?
Loss of sodium in the urine
To what do atrial natriuretic peptides respond?
Increased blood volume
Stretch of cardiac atria -> causing ANP secretion -> inhibition of aldosterone (does the opposite of Angiotensin II)
in the Kidney:
1) Afferent arterioles dilated and efferent constricted -> increase of GFR
2) Reabsorption of Na reduced
3) Inhibits renin release
–> all those cause increased Na excretion
What does BNP do?
similar to ANP
-released to respond to the stretch of the ventricular muscle
-enhance Na and water excretion
-BNP and ANP are broken down by neprilysin
How does the body react to excess water?
The hypothalamic osmotic receptor will fire less -> less vasopressin in plasma -> fewer aquaporins that reabsorb H2O -> more H20 stays in urine and gets excreted
How does the body to the reduced amount of water?
There will be less plasma volume and less venous, atrial, and arterial pressure -> recognized by Posterior Pituatiary (baroreceptors: increase Vasopressin secretion -> increase of water reabsorption through aquaporins -> less H2O excretion
What other mechanism has the body to counteract reduced water amounts?
-sympathetic NS activation
-activation of renin/angiotensin and aldosterone
How does the body compensate for severe sweating?
1) Sodium: low plasma volume will cause the decrease in GFR and activation of aldosterone
2) H2O: high plasma osmolarity (low H2O) will activate vasopressin -> activates aquaporins and reduces H2O excretion
How is thirst stimulated?
1) Low plasma volume detected by Barorecptors -> activation of Angiotensin II
2) Baroreceptors itself
3) High plasma osmolarity detected by osmoreceptors
4) Dry mouth, throat
-Metering of water intake in GI reduces thirst
Where and how does K+ reabsorption occur?
Loop of Henle (principal cells), though NKCC pumps
How is K+ secretion stimulated/regulated?
a small increase of extracellular K+ will stimulate the Na+K-ATPase pump and cause K+ secretion into urine and excretion from the urine
What is a major stimulus of aldosterone?
An increase in K+ plasma level
Aldesterone inccreases N+ reabsorption and K+ secretion + excretion
How else is K+ secretion stimulated?
Number of Na+ in tubule lumen (urine) -> if it is high there it will go into the principal cell (collecting duct) -> and it forces K+ out of the cell either on the apical side (into the urine) or basolateral side
also, Aldosterone (released by the adrenal cortex) causes K+ secretion
How does N+ get into the cell and K+ out of the cell?
NKCC pumps
Na+ reabsorption at the expense of K+ secretion
How is the number of Na+ outside of the cell (tubule lumen - urine) increased?
Through Loop diuretics (drugs) blocking NKCC pumps
Why must K+ be strongly regulated?
They affect the resting membrane potential of excitable cells
Angiotensin II role in K+ secretion:
low plasma volume causes Angiotensin II release -> causing the adrenal cortex to release aldosterone -> aldosterone increases Na+ reabsorption and K+ secretion + excretion
How is Ca and PO4 level regulated?
By PTH
-causes more reabsorption of Ca++ and inhibits reabsorption of PO4 in the kidney
-activates 1,25 dihydroxy Vitamin D (active Vit D) which increases absorption of Ca and PO4 in the intestine
Where does reabsorption of Ca and PO4 occur?
-Proximal convoluted tubule
-Fine-tuning in distal convoluted tubule under control of PTH
