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Phys3 Reg: Na,H2O,BP

Phys3 Renal Regulation of NaCl,H2O,Vol & BP

Hyponatremia Too much water. **over dilutes the solutes in the ECF causing hyposmolality.
Hypernatremia Too little water
Too much sodium Edema
Too little sodium volume depletion.
Difference between osmolality and volume regulation? 1.Osmolality reg: via Water regulation. 2.Volume reg: via Na + Excretion or Retention.
What are the intrarenal baroreceptors? Renin-producing granular cells. **sense a Dec in renal afferent pressure.
What is the relationship b/w flow at the Macula densa and renin secretion by the granular cells? INVERSELY related. **High flow at macula densa, Low renin secretion. **Low flow at macula densa, high renin secretion.
What 3 things influence the granular cells' secretion of renin? 1.SNS. 2.Intrarenal baroreceptors. 3.flow at Macula densa
Granular cells response to Hemorrhage (Dec BP via Dec BV) Increase Renin secretion due to: 1.Inc SNS. 2.Dec baroreceptor firing. 3.Dec flow to macula densa cells.
What does an Increased Renin secretion cause? 1.Inc plasma [Ang II]. 2.Inc plasma [Aldosterone]
In the intermediate term, What hormone is responsible for maintaining BP during severe hypotension? Ang II. Causes greater efferent vasoconstriction which leads to Inc P(gc) and maintaining GFR.
What does long term BP control depend upon? Controlling the amount of Na and water in ECV.
what would the kidneys do if Low ECV reabsorb Na & water.
what would the kidneys do if high ECV excrete more Na & water.
Na excretion depends on 2 variables: 1.GFR. 2.Na reabsorbed.
How would nsaids effect the RAAS system? Could endanger the kindey b/c they decrease prostaglandins which normally have a protective effect over the renal arterioles. **they normally cause VD to leasen the Ang II & SNS VC.
Influences of Na reabsorption? 1.Ang II Inc Na/H exchanger in PT. 2.SNS Inc Na/K ATPase in PT. 3.Ang II Inc Na reab in vasa recta loop. 4.High Vol & BP Dec Ang II: Dec Na transporters in PT, Dec passive Na reab in thin AL. 5.ADH Inc ENaC in CCD. 6.Aldost. Inc Na reab in CCD. 7.AN
Is there as much Na & Water excretion during High renal P, Low BV as there is in High renal P, high BV? NO.
Effects of Aldosterone on CCD 1.Inc basolateral Na/K ATPase. 2.Inc basolateral SA. 3.Inc # of Na/K pumps. 4.Inc Na channels. 5.Inc K+ cell->Lumen driving force & conductance.
Body wide effects of AngII 1.Inc aldosterone release from adrenal cortex. 2.Dec Na excretion from PT. 3.Inc SVR via peripheral arterioles. **Inc BV & MAP
Influences on Aldosterone release 1.Ang II. 2.HyperKalemia. **ANP INHIBITS release.
ADH affect on Na excretion DEC excretion, Inc reabsorption in CCD and thick ascending limb.
Stimulus for ADH release 1.Inc plasma osmolality. 2.Dec BV. 3.Plasma AngII. 4.Dec MAP
ANP affect on Na excretion 1.Kidney excrete more Na & water. 2.Inhibits renin, ADH, & Aldosterone. 3.VD renal arteries.
Osmoregulation sensors 1.Hypothalamic osmoreceptors.
Volume regulation receptors 1.Macula densa. 2.Afferent arteriole (granular cells). 3.Atria. 4.Carotid sinus. **Inc signals from 3 & 4 Dec ADH.
glomerulotubular balance (GTB) The nephron tries to excrete a constant fraction. **therefore, Inc filtration: Inc absolute Na excretion. Dec filtration: Dec absolute Na excretion.
What does GTB do to Na excretion in response to a GFR change? Blunts it
Water excretion 1.Follows Na in PT. 2.Reabsorbed in descending loop. 3.No reabsorption in ascending loop. 4.No reabsorption in DCT. 5.CD: depends on ADH. **some reabsorption in IMCD w/out ADH.
Created by: WeeG



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