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Phys3 Reg: Na,H2O,BP
Phys3 Renal Regulation of NaCl,H2O,Vol & BP
Question | Answer |
---|---|
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. |