Renal Physiology 3 Flashcards
What are the principals of salt and water homeostasis?
- regulation of ECF volume & osmolarity is achieved by controlling sodium and water
- Total body content of Na+ is primary determinant of ECF, hence plasma volume & adequacy of circulation or ECV
- Hence Na+ excretion is regulated in response to signals reflecting the adequacy of the circulation or effective circulating volume (ECV)
- Na+ excretion is determined by the kidney
- Primary effector is renin angiotensin aldosterone system (RAAS) system which responds to drop in BP
- Normal plasma osmolarity is 290 mOsm/kg The major ion that determines the ECF osmolarity is Na+ concentration
- Na concentration (osmolarity) is not the same as total body Na+ & is the function of water balance
- Is mainly regulated by signals affecting osmolarity
How is ADH synthesized?
In the hypothalamus & stored in the posterior pituitary. Most important trigger for release of ADH is
- increased plasma osmolarity
- 2^0 trigger is loss of ECF volume >10% via a baroreceptor reflex
-is released from posterior pituitary
Normal plasma osmolarity is 290 mOsm /L
Summarize plasma osmolarity
Deprive of water leads to increased plasma osmolarity—> stimulates osmoreceptors in anterior hypothalamus
This not only leads to thirst and increased water intake, but also increased ADH secretion from posterior pituitary
- Water permeability of principal cells (late distal tubule and collecting duct)
- increased water Reabsorption
- increased urine osmolarity and decreased urine volume
- the previous step and increased water drinking lead to decreased plasma osmolarity toward normal
Summarize volume regulation
There are number of sensors that regulate the volume
- They are located in different areas (carotid, aort8c arch, JGA apparatus & right atria)
- They are sensitive to changes in pressure
- JGA is one of the dominant sensor located in the kidney. It is sensitive to drop in pressure.
- Restores volume by activating Renin Angiotensin aldosterone system (RAAS)
- ANP is released in response to increased pressure
What are the effects of low ECV on the kidneys?
- Low blood pressure lowers GFR which decreases NaCl transport across macula densa tubule
- paracrine then stimulate granular cells of afferent arteriole to release renin
- Direct pathway is when blood pressure stimulate granular cells of afferent arterioles to release renin
- Low blood pressure- cardiovascular control center detects low blood pressure which increases sympathetic activity and leads to granular cells of afferent article releasing renin
Explain the functioning of aldosterone
- Aldosterone combines with a cytoplasmic receptor
- Hormone-receptor complex initiates transcription in the nucleus
- New protein channels and pumps are made
- Aldosterone-induced proteins modify existing proteins
- Result is increased Na+ Reabsorption and K+ secretion
How does angiotensin 2 defend the effective circulating volume in several ways?
Angiotensin 2-ADH release increases water retention
-stimulates thirst
-vasoconstriction (systemic and intra renal)
Increased proximal tubule Na+ Reabsorption
Stimulate aldosterone which increases distal tubule Na+ Reabsorption
Summarize atrial natriuretic peptide and AGII- high ECV
Actions:
- AGII vasodilation afferent arterioles & constricts efferent arterioles thereby increasing GFR
- ANP contributes to small increases in GFR
- This along wil Agll promotes increased excretion of sodium
- ANP inhibits Na+ Reabsorption directly at the medullary CD
Summarize Regulation of Extracellular fluid volume
- Regulation of ECF volume is linked to Na+ Reabsorption
- This in turn affects water Reabsorption. This in turn affects ECF volume
- Falls in blood pressure activate renal mechanisms to increase Na+ Reabsorption and water Reabsorption
- The main player in these responses is the Renin Angiotensin Aldosterone system (RAAS) and sympathetic nervous system
