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8 - Renal Regulation of Na, ECV and BP


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What is the basic premise of GT balance?
Changes in GFR are matched by changes in NaCl and water reabsorption; i.e. the nephron reabsorbs a constant fraction of filtered salt and water rather than an absolute quantity.
How does reabsorption of NaCl and water increase when GFR increases?
Greater GFR means more protein-free fluid is filtered out of the plasma entering the peritubular capillaries, which acts to raise its COP. This favors a greater uptake of water and, by extension, NaCl.
In what segment of the nephron is resetting of GT balance centered?
The proximal convoluted tubule.
What effect does increased Na+ intake have on the reabsorption of NaCl and water by the peritubular capillaries?
Increased Na+ leads to increased ECV through water retention. This increases MAP and thus hydrostatic pressure in the peritubular capillaries. Also, the COP of plasma is reduced. Both of these factors lead to decreased reabsorption.
How is reabsorption affected in times of lowered ECV?
MAP, and thus hydrostatic pressure in the peritubular capillaries is decreased. Also, low volume means that COP of plasma is increased. Both of these factors favor increased reabsorption.
What is meant by a "positive balance"?
Intake of a substance exceeds its output.
What is meant by a "negative balance"?
Output of a substance exceeds its intake.
How are renal mechanisms involved in an acute drop of 10% in ECV?
They are largely not involved - MAP is maintained by the baroreceptor reflex. Renal mechanisms are involved in longer-term maintenance of ECV and BP.
What is sensed by granular cells?
Renal perfusion pressure.
What is the overall action of ANP? Where is this substance synthesized?
*Promotion of Na+ excretion
*synthesized in the atria
What is the action of ANP in the distal tubule and collecting ducts? In the afferent arterioles?
*direct inhibition of ENaC and indirect inhibition of Na+/K+ ATPase
*inhibits release of renin and causes dilation of these arterioles
What is the basic overall action of sympathetic innervation of the kidneys?
Increase reabsorption of Na+ and decrease excretion of Na+ and water.
On which glomerular arterioles does sympathetic innervation have the greater effect - afferent or efferent?
Exerts a greater effect on afferent arterioles.
When ECV is decreased, what are the two specific effects of sympathetic innervation on the kidneys?
*constriction of the afferent arterioles to decrease GFR
*stimulation of Na+/H+ antiporter to increase Na+ reabsorption
How do ECV and blood pressure influence the release of renin?
Decreases in both cause stimulation of renin release.
Give the steps between release of renin and the appearance of angiotensin II in circulation.
1.Renin released
2.Renin catalyzes conversion of angiotensinogen to angiotensin I
3.ACE catalyzes the conversion of angiotensin I to angiotensin II
What is the action of angiotensin II on total peripheral resistance?
Angiotensin II is a potent vasoconstrictor and thus raises total peripheral resistance.
On which arterioles does angiotensin II have the greater effect - afferent or efferent?
Angiotensin II has a greater vasoconstrictive effect on the efferent arterioles.
How does the arteriolar constriction caused by angiotensin II cause an increase in reabsorption?
Ang-II contricts the efferent arterioles which does cause an increase in GFR, but also a decrease in the hydrostatic pressure in the peritubular capillaries. This means that the plasma entering the capillaries has high COP and low hydrostatic pressure, both of which favor reabsorption.
Other than vasoconstriction, what are three effects that angiotensin II have?
*stimulation of Na+/H+ antiporter in the PCT
*stimulation of release of ADH and aldosterone
*stimulation of thirst centers
How does the kidney prevent cross-stimulation of the mineralocorticoid receptor by cortisol?
Secretion of enzymes that catalyze the conversion of cortisol to cortisone, which is unable to activate the MR.
There is genereally a ~90 minute latency period between the appearance of aldosterone in circulation and evidence of its action. Why is this?
Aldosterone is a steroid hormone and as such its effects are mediated by transcriptional and translational changes in protein synthesis. Changes of this type take longer to enact.
How does aldosterone affect ENaC? What effect does this have on Na+ reabsorption?
Aldosterone increases ENaC activity, which promotes Na+ reabsorption.
What is the effect of aldosterone on K+ reabsorption?
Aldosterone promotes K+ secretion, thus its net reabsorption is inhibited.
What other organ system is affected by aldosterone? What is the effect?
Aldosterone stimulates increased Na+ absorption in the large intestine and colon.

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