Lecture 8 - Blood pressure in the kidney Flashcards
How does hypotension affect the kidney
- Reduced blood flow to the kidney detected by low pressure baroreceptors
- Interpreted as a reduction in ECF
- The macula densa cells release prostaglandins which cause the afferent arteriole to dilate (tubuloglomerular feedback system).
- More Na+ , Cl- and water is retained via RAAS and the myogenic response.
- Increase renal blood flow
Main responses to hypotension in the kidney
RAAS
Sympathetic NS
Prostaglandins
ADH
RAAS
- Liver produces angiotensinogen which is converted to angiotensin I by renin which is produced by the granular cells of the kidney and released in response to hypotension.
- Ang I is converted to ang II by the angiotensin converting enzyme (ACE) in lungs.
- Ang II acts on the adrenal gland to release aldosterone (steroid hormone)
- Aldosterone acts on the collecting ducts to retain water, increasing BP.
ACE inhibitors
Inhibits ACE therefore less angiotensin I is converted to angiotensin II
Can cause dry cough due to bradykinin accumulation
Statins
Inhibit the effects of angiotensin II so less aldosterone is produced.
Spironolactone
Inhibits the effect of aldosterone in DCT
Inhibits ROMK in PCT
Sympathetic NS control of hypotension
Hypotension detected by baroreceptors
- Beta 1 adrenergic nerve stimulates renin release which stimulates RAAS. (slow)
- Decreased SAN threshold therefore increased HR
- Increased myocardial contractility which increases stroke volume
- Vasoconstriction which increases TPR
Aldosterone
Produced by the zona glomerulosa of the adrenal gland
Steroid hormone
- In the DCT, aldosterone stimulates the Na+/K+ pump in the principal cells.
- More Na+ is reabsorbed and thus water is reabsorbed too
- More K+ is secreted therefore there is a risk of hypokalaemia.
Conditions that reduce perfusion pressure with ECF volume intact
Heart failure
Liver cirrhosis
Nephrotic syndrome
Renal artery stenosis
Renal response to hypertension
- Increased kidney perfusion
- Decrease in aldosterone secretion and ANP released.
- Decrease in ECF volume
- Decreased BP
Oedema
Excessive secretion of fluid in the interstitium.
Can be caused by excess salt and water retention by the kidney
Secondary hypertension
Renal artery stenosis
Coarctation of the aorta
Primary hyperaldosteronism (Conn’s syndrome)
Cushing’s syndrome
3 mechanisms that releases renin from the kidney
- Direct sympathetic stimulation of the JGA
- Reduced renal blood flow detected by baroreceptors in the JGA
- Reduced NaCl to the macula densa cells
Angiotensin II
Increases synpathetic activity
Increases reabsorption of Na+ and water retention
Stimulates the adrenal glands to release aldosterone from the zona glomerulosa
Arterioriole vasoconstriction - increase TPR
Increases the secretion of ADH from the pituitary gland posterior lobe
What does aldosterone stimulate?
DCT:
- Upregulation of Na+/K+ pump on the basolateral membrane
- Upregulates Na/Cl cotransporter
- Stimulates secretion of K+ into the tubule
Collecting duct::
- Upregulates Na+ channels in the collecting duct and colon
- Stimulates H+ secretion in the collecting duct